Biotechnology and Diagnostics Initiating Coverage September 7, 2018 BUY Kevin DeGeeter; [email protected] 212.409.2027

CYCLACEL PHARMACEUTICALS, INC. CYC065 Shows Promise in Mcl-1 Regulation; Initiate Coverage with Buy & $6.25 PT

CYCC (NASDAQ) We are initiating coverage of Cyclacel Pharmaceuticals, Inc. (Nasdaq: CYCC) with Company & Market Data a BUY rating and $6.25 price target. We believe CYC065, the company’s CDK Closing Price (as of 09/06/2018): $1.43 2/9 inhibitor, has demonstrated clear signs of activity against the Mcl-1 pathway, Rating: BUY which has long been viewed as an attractive target for treatment of hematologic Price Target: $6.25 52 Week Range: $1.28 - $2.27 malignancies. Our investment thesis is based on the following assumptions: 1) CDK9 Shares Outstanding (MM): 12.0 is a validated approach to regulating the anti-apoptotic Mcl-1 protein in CLL, AML and Market Capitalization (MM): $17 other hematologic malignancies, 2) Phase I data has demonstrated CYC065 provides Cash (MM): $19.8 prolonged suppression of Mcl-1 expression following a single dose, and 3) additional Fiscal Year End: Dec regulation of CDK2 may offer synergy based on exploratory preclinical findings. If Estimates CYC065 maintains an acceptable safety profile – a key challenge for first-generation EPS 2017A 2018E 2019E CDK2/9 inhibitors – in our view, CYC065 will be an important option for combination 1Q $(0.44) $(0.13)A — therapy in 2nd line hematologic malignancy populations with peak sales potential of 2Q $(0.55) $(0.20)A — $650M+. In terms of catalysts, we view mid 2019 presentation of top-line Phase II data for 3Q $(0.21) $(0.18) — CYC065 in combination with venetoclax in patients with relapsed/refractory CLL as the 4Q $(0.17) $(0.21) — most significant milestone. While Mcl-1 has been linked to disease activity in a range of Full Year $(1.10) $(0.71) $(0.91) malignancies, we view second line CLL as an attractive path to market based on 1) more Revenue (MM) 2017A 2018E 2019E homogenous disease biology than AML, 2) preclinical data suggesting potential synergy 1Q $0.0 $0.0A — with venetoclax, and 3) unmet need with median survival around 2 years. Our $6.25 price 2Q $0.0 $0.0A — 3Q $0.0 $0.0 — target is based on a DCF analysis assuming a 32% discount rate, 20.3 million shares on a 4Q $0.0 $0.0 — fully diluted basis, terminal year (2025) FCF of $177.1M and 13% long-term growth rate. Full Year $0.0 $0.0 $0.0 • CYC065 CLL Combo with Venetoclax –$650M Peak Sales: CYCC has submitted a protocol for IRB approval to evaluate CYC065 in combination with venetoclax for Cyclacel is a clinical stage biotechnology company treatment of 2nd line CLL patients with data available as early as mid 2019. We expect developing oncology drugs based on cell cycle patients to be titrated up to the prescribed dose of venetoclax from a starting dose of regulation, transcriptional regulation and DNA 20mg. Once the patient reaches steady state, we expect CYC065 to be added at a damage response. The company’s research schedule of a 4-hour infusion once every 3 weeks. We encourage investors to focus activity is focused on CYC065, a CDK2/9 inhibitor primarily on tolerability including neutropenia and tumor lysis syndrome. In terms of in Phase I development for relapsed/refractory efficacy, we believe the unmet need in 2nd line CLL is for deeper responses (i.e., more CLL. The company's early-stage pipeline includes CRs) rather than higher ORR or PFS. Durability data will likely mature in 2H19 and CYC140, a PLK1 inhibitor. The Berkeley Heights, 2020 providing additional clinical news flow from the study. NJ-based company retains global rights to each of its drug candidates. • Targeted Agents for CLL Supports Combination Strategy: With growing acceptance of BTK inhibitors such as ibrutinib in the frontline setting and potential of the BCL-2 inhibitor venetoclax to be established as the standard of care in second line setting, we believe 1) chemotherapy will be increasingly less relevant to treatment of CLL, at least in the U.S., and 2) combination regimens of two or more targeted agents may offer higher complete response rates effectively “curing” more frontline patients and providing more durable response in the second line setting. • Tolero Offers Attractive Benchmark for Strategic Value of CDK9: Sumitomo acquired Tolero Pharmaceuticals for $200M at closing and $580M in milestone payments based on the CDK9 inhibitor alvocidib. Alvocidib was entering Phase II development when Sumitomo acquired the asset. We view CYC065, which could enter Phase II development in CLL in 2H18, as potentially differentiated from alvocidib based on both IV and oral dosing compared to IV dosing with alvocidib, potential for better tolerability and different paths to regulatory approval in AML (alvocidib) and CLL (CYC065).

Disclosures￿and￿Analyst￿Certifications￿can￿be￿found￿in￿Appendix￿A.

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Member: NYSE, NYSE American, NYSE Arca, FINRA, all other principal exchanges and SIPC Kevin DeGeeter 212.409.2027 Cyclacel Pharmaceuticals, Inc. (CYCC)

INVESTMENT THESIS Initiating Coverage with a BUY Rating and $6.25 Price Target

We are initiating coverage of Cyclacel Pharmaceuticals, Inc. (Nasdaq: CYCC) with a BUY rating and $6.25 price target. We believe CYC065, the company’s CDK 2/9 inhibitor, has demonstrated clear signs of activity against the Mcl-1 pathway, which has long been viewed as an attractive target for treatment of hematologic malignancies. Our investment thesis is based on the following assumptions: 1) CDK9 is a validated approach to regulating the anti-apoptotic Mcl-1 protein in CLL, AML and other hematologic malignancies, 2) Phase I data has demonstrated CYC065 provides prolonged suppression of Mcl-1 expression following a single dose, and 3) additional regulation of CDK2 may offer synergy based on exploratory preclinical findings. If CYC065 maintains an acceptable safety profile – a key challenge for first-generation CDK2/9 inhibitors – in our view, CYC065 will be an important option for combination therapy in 2nd line hematologic malignancy populations with peak sales potential of $650M+.

In terms of potential catalysts, we view mid 2019 presentation of top-line Phase II data for CYC065 in combination with venetoclax in patients with relapsed/refractory CLL as the most significant milestone. While Mcl-1 has been linked to disease activity in a range of malignancies, we view second line CLL as an attractive path to market based on 1) more homogenous disease biology than AML, 2) preclinical data suggesting potential synergy with venetoclax, and 3) unmet need with median survival around 2 years. Our $6.25 price target is based on a DCF analysis assuming a 32% discount rate, 20.3 million shares on a fully diluted basis, terminal year (2025) FCF of $177.1M and 13% long-term growth rate.

CDK9 Inhibition Offers Validated Path to Evaluate Mcl-1 Inhibition We believe data from prior studies of pan-CDK inhibitors (dinaciclib) and selective CDK9 inhibitors (alvocidib) have validated CDK9 as clinically relevant in patients with elevated Mcl-1 expression. By way of background, CDK9 is a subunit of the positive transcription elongation factor b (P-TEFb), also comprising CycT1 or CycT2, and is required for transcription elongation by RNAPII. Transcriptional regulation is tightly controlled by CDK9 via phosphorylation of residues on the C-terminal domain (CTD) of RNAPII, which downregulates activity of suppressors that inhibit RNAPII activity. Inhibition of CDK9 mediated phosphorylation of the CTD RNAPII results in reduced levels of antiapoptotic proteins such as Mcl-1. Short-term CDK9 inhibition suppresses Mcl-1 transcription and rapidly depletes Mcl-1 protein (due to short half-life of the protein) resulting in caspase activation and cell death in Mcl1-dependent cancer cells. While CDK4/6 inhibitors used to treat breast cancer have not been amenable to biomarker selection, in our view, Mcl-1 expression may serve as an important predictor of response to CDK9 inhibitors such as CYC065.

Addition of CDK2 Inhibition Offers Differentiation from Other CDK9 Inhibitors We believe CYC065 is the only compound currently in clinical development combining selective inhibition of CDK2 and CDK9. In an article published in the January 2018 issue of Molecular Oncology entitled “Molecular profiling and combinatorial activity of CCT068127: a potent CDK2 and CDK9 inhibitor,” the authors concluded CDK2 expression may regulate CDK9 through a feedback loop, which suggests targeting both may be necessary for sustainable suppression of Mcl-1. If this hypothesis is borne out in clinical development, CYC065 may offer superior potency over selective regulation of only CDK9. Our base case assumes potency differences for molecules in the class will be driven primarily by level of CDK9 target engagement and compliance/tolerability of the regimen.

CLL Combo Study with Venetoclax Offers Biggest Upside Opportunity CYCC has submitted a protocol for IRB approval to evaluate CYC065 in combination with venetoclax for treatment of 2nd line CLL patients with data available as early as mid 2019. We expect patients in the study to be titrated up to the prescribed dose of venetoclax from a starting dose of 20mg. Once the patient reaches steady state, we expect CYC065 to be added at a schedule of a 4-hour infusion once every 3 weeks. We encourage investors to focus primarily on tolerability including neutropenia and tumor lysis syndrome. In terms of efficacy, we believe the unmet need in 2nd line CLL is for deeper responses (i.e., more CRs) rather than higher ORR or PFS. Durability data will likely mature in 2H19 and 2020 providing additional clinical news flow from the study.

Page 2 Kevin DeGeeter 212.409.2027 Cyclacel Pharmaceuticals, Inc. (CYCC)

Growing Use of Targeted Agents for CLL Supports Combination Therapy Strategy Until five years ago chemotherapy in combination with CD20 agents was the primary treatment option for most CLL patients both in frontline setting and for relapse/refractory disease. With growing acceptance of BTK inhibitors such as ibrutinib in the frontline setting and potential of the BCL-2 inhibitor venetoclax to be established as the standard of care in second line setting, we believe 1) chemotherapy will be increasingly less relevant to treatment of CLL, at least in the U.S., and 2) combination regimens of two or more targeted agents may offer higher complete response rates effectively “curing” more frontline patients and providing more durable response in the second line setting.

Tolero Offers Attractive Benchmark for Strategic Value of CDK9 In December 2016 Sumitomo agreed to acquire privately held Tolero Pharmaceuticals for $200M at closing, $430M in clinical and regulatory milestones and an additional $150M related to future sales milestones. While Tolero had 6 molecules in early-stage development at the time of the transaction, Sumitomo noted the CDK9 inhibitor alvocidib was the primary strategic rationale for the deal. Alvocidib was entering Phase II development when Sumitomo acquired the asset. We expect CYC065, which should enter Phase II development in CLL during 2H18, as potentially differentiated from alvocidib based on both IV and oral dosing compared to IV dosing with alvocidib, potential for better tolerability and different paths to regulatory approval in AML (alvocidib) and CLL (CYC065).

CYC065 – Validated Target with Peak Sales Potential of $650M+ Our CYC065 revenue forecast focuses on relapsed/refractory CLL based on 1) significant unmet need with median survival in refractory population of less than two years, 2) potential to combine with other targeted agents such as BCL-2 inhibitors and 3) good treatment options currently available in the frontline setting. About 60,300 Americans are diagnosed with leukemia each year, according to the American Cancer Society. Roughly 30% to 35% of leukemia patients are diagnosed with CLL for annual incidence rate of 20,940. Complete response rates for frontline therapy are only about 20% and roughly 80% of patients eventually develop refractory or relapsed disease, which suggests an addressable market of roughly 16,800 patients. In the absence of clinical data for CYC065 the duration of response is difficult to forecast but we view 7 cycles of therapy as a reasonable minimum threshold for a commercially viable drug, which implies around $87,500 per patient. We expect the company to eventually partner CYC065 for ROW in exchange for economics equivalent to 13%-18% royalty on net sales (point estimate of 15%). We forecast peak sales in 2027 of $540.9M on a reported basis including $526M in U.S. sales, $99.6M from international markets and international royalties of $14.9M.

Pediatric Neuroblastoma Offers Favorable Upside / Downside Profile We encourage investors to focus on advancement of CYC065 into clinical development as a monotherapy for pediatric neuroblastoma, which, in our view, offers an accelerated path to market based on high prevalence of MYC-M overexpression and potential to win regulatory approval with positive data in 25-40 patients. CYCC is working with a clinical trials consortium with a specialty in pediatric neuroblastoma to evaluate the role of CYC065 IV in pediatric neuroblastoma in patients with MYC-M overexpression. Preclinical studies suggest MYC-M overexpression may be mutually exclusive from TRK gene fusions in most patients, which suggests the target population may not be candidates for larotrectinib. As such, this patient population represents a significant unmet medical need. Management estimates roughly half of patients have MYC-M amplification. The American Cancer Society estimates roughly 800 neuroblastoma patients are diagnosed each year in the U.S. with 90% of cases diagnosed by age 5 years. The literature suggests 40-50% of these patients have MYC-M amplification. We expect CYCC to explore kicking off clinical development in the next 12 months.

Page 3 Kevin DeGeeter 212.409.2027 Cyclacel Pharmaceuticals, Inc. (CYCC)

VALUATION: $6.25 PRICE TARGET

Our $6.25 price target for shares of CYCC is based on a discounted cash flow (DCF) model for sales of CYC065 for the treatment of relapsed/refractory CLL. We do not include potential revenues from use in cyclin E-mediated ovarian cancer, breast cancer and other solid tumors.

Our model calls for the company to commercialize CYC065 in the United States with a field sales force of 35-40 reps. We expect CYCC to seek commercial partners outside the U.S. with the company receiving economics equivalent to a net royalty of 15%-18%. We expect the company to achieve profitability in 2023 or 2024 and begin paying taxes in 2025 at an effective tax rate of 30%. Our forecast calls for CYCC total revenue of $381M for 2025 (last year of our DCF model) with roughly 80% of gross revenue from U.S. sales and the remainder from international markets. For the final year of our DCF valuation we forecast free cash flow of $177.1M driven by sales of CYC065. Our DCF model assumes a 32% discount rate, long term revenue growth rate of 13% and share count of 20.3 million on a fully diluted basis.

Table 1. DCF Assumptions Commercial DCF Assumptions Discount rate 32% Long-term revenue growth 13% Terminal year 2025 Fully diluted share count (in millions) 20.3 Source: Ladenburg Thalmann estimates and company reports

We view a 32% discount rate, which is 400 basis points higher than our typical discount rate for a company with a lead program entering Phase II development, as appropriate given 1) limited validation of CDK9 inhibition as a clinically important target for hematologic malignancies, 2) limited experience of CYCC management in commercializing biotech oncology drugs and 3) significant capital requirements to commercialize CYC065 for multiple indications relative to cash balances totaling $19.8M at the end of June.

Our 13% long term revenue growth rate is 200 basis points below our standard long-term growth rate for biotechnology companies. We believe the growth rate is appropriate given the limited pipeline beyond CYC065 focused primarily on the PLK1 inhibitor CYC140 and relatively modest base investment in R&D totaling $4.2M in 2017.

Our share count of 20.3 million assumes cash conversion of roughly 8.2 million options and warrants. Our model calls for current cash balances to fund operations into 1H20 with an incremental capital requirement of roughly $60M-$100M to achieve profitability.

Table 2. Overview of DCF Model

Cyclacel Pharmaceuticals Discounted Cash Flow Assumptions ($ in millions) 2018E 2019E 2020E 2021E 2022E 2023E 2024E 2025E TERMINAL Operating profit ($9.3) ($10.9) ($15.3) ($22.3) ($31.6) $9.1 $137.3 $282.0 Depreciation & amortization 0.0 0.0 0.0 0.0 0.0 0.0 0.0 0.0 Taxes 0.0 0.0 0.0 0.0 0.0 0.0 0.0 (84.8) Interest income - net 0.8 0.1 0.0 (0.0) (0.1) (0.2) (0.1) 0.5 Change in working capital (1.0) 0.3 0.7 1.2 1.5 (9.2) (21.6) (20.7) Capital expenditures (0.0) 0.0 0.0 0.0 0.0 0.0 0.0 0.0 Total free cash flow ($9.5) ($10.6) ($14.5) ($21.2) ($30.2) ($0.3) $115.6 $177.1 $889.9

Revenue growth rate NA NA NA NA NA NA 215% 73% 13%

Discount rate 32% 32% 32% 32% 32% 32% 32% 32% 32% Discount factor 1.0 0.8 0.6 0.4 0.3 0.2 0.2 0.1 0.1

Discounted cash flow ($9.5) ($8.0) ($8.3) ($9.1) ($9.8) ($0.1) $21.5 $24.8 $124.8 Source: Ladenburg Thalmann estimates

Page 4 Kevin DeGeeter 212.409.2027 Cyclacel Pharmaceuticals, Inc. (CYCC)

POTENTIAL NEAR-TERM EVENTS

Over the next 12-18 months we view presentation of top-line Phase II data for CYC065 in combination with venetoclax in patients with relapsed/refractory CLL as the most significant milestone. Additionally, we encourage investors to focus on advancement of CYC065 into clinical development as a monotherapy for pediatric neuroblastoma, which offers an accelerated path to market based on the high prevalence of MYC-M overexpression in the population. Furthermore, preclinical studies suggest MYC-M overexpression may be mutually exclusive from TRK gene fusions, which suggests the target population may not be candidates for larotrectinib.

Additional news flow includes 1) data in 4Q18 from Part 2 of the Phase I CYC065 monotherapy study exploring a more frequent dosing schedule of 2 days per week for 2 weeks of a three-week cycle compared to a single 4-hour infusion every 3 weeks in the Part 1 dose-escalation cohort, 2) initiation of an investigator sponsored Phase Ib/II study of an approved PARP inhibitor with sapacitabine in patients with BRCA mutant breast cancer, 3) discussions with regulatory authorities regarding next steps following negative results from the Phase III SEAMLESS study of sapacitabine in AML and 4) filing of an IND for the PLK1 inhibitor CYC140.

Table 3. Near Term Events Expected Near-Term Events Event Time Importance Updated CYC065 Phase I data for advanced cancers 2H18 Moderate Initiate CYC065 Phase II in combination with venetoclax for r/r CLL 2H18 Low Begin Phase Ib/II study of CYC065 for pediatric neuroblastoma 2H18 Low Meet with regulators to discuss SEAMLESS data 4Q18 Moderate File IND for CYC140 2019 Low Topline data for CYC065 Phase II in combination with venetoclax for r/r CLL Mid 2019 High Source: Company reports and Ladenburg Thalmann estimates

CORPORATE BACKGROUND AND BUSINESS MODEL

The predecessor company, Xcyte Therapies, was formed in 1997 but the current business is based on the 2005 merger of the financial assets from Xcyte with operating assets from Scottish biotech start up Cyclacel Group PLC, which was focused on developing oncology drugs based on scientific expertise in cell cycle regulation, transcriptional regulation and DNA damage response. The company maintains corporate headquarters in New Jersey and a research group in Dundee, Scotland.

Over the past five years CYCC has progressively moved away from translational research on novel drug targets and focused on clinical development. The company now relies on a semi-virtual development model using contract manufacturing groups to produce drug product and a web of third party contractors to support clinical trials. CYCC has typically retained global rights to each of its pipeline programs. Given the unencumbered pipeline, in our view, the company could eventually be an attractive acquisition candidate to a global biotechnology and pharmaceutical company.

Following the failure of sapacitabine in a Phase III acute myeloid leukemia (AML) study in 2017, management refocused the pipeline around two early-stage assets – the CDK2/9 inhibitor CYC065 and the PLK1 inhibitor CYC140. We view these two programs as the last important novel drug candidates developed within CYCC and expect any future expansion of the pipeline to be driven by in-licensing or acquisitions.

Of the two remaining core assets, we assign nearly all of the company’s value to CYC065, which is a CDK 2/9 inhibitor that may provide an attractive strategy for indirectly regulating Mcl-1 activity. The compound entered Phase I development in 2017 and is being evaluated in a Phase I clinical trial of patients with advanced cancers mediated by Mcl-1, MYC or cyclin E. We expect the drug to be used primarily in combination regimens, potentially with BCL-2 inhibitors such as venetoclax.

Page 5 Kevin DeGeeter 212.409.2027 Cyclacel Pharmaceuticals, Inc. (CYCC)

PIPELINE OVERVIEW

CYCC is developing a pipeline of oncology drugs based on translational research of the role of cell cycle biology on cancer cell growth and apoptosis. While the company was founded based in part on the work of academic collaborators, in our view, CYCC currently has limited resources allocated to translational work against novel drug targets and is primarily focused on clinical development of its lead drug candidates.

The company currently highlights eight internal programs and three partnered programs from its pipeline (see Figure 1 below). However, we expect two internal programs to account for nearly all of the potential value creation: 1) CYC065 in combination with venetoclax for CLL and other hematologic malignancies and 2) CYC065 in cyclin E overexpressing ovarian and breast cancer patients.

We do not expect the company to make additional internal investments in sapacitabine following the failed Phase III program in AML and are circumspect regarding the potential of CYC140 and of PLK1 inhibition as an attractive target for future development.

Figure 1. CYCC Development Pipeline Development Pipeline Program Indication Preclinical Phase I/Ib Phase II Pivotal Commercial Rights

Solid Tumors (FIH) RPh2D Worldwide Mcl-1: RR LL ± Bcl inhibitors CYC065+v enetoclax RR CLL CYC065 (IV + oral CDK2/9 Cyclin E: Ovarian, HER2+ BC inhibitor) CYC065 Ov arian DDR: BRCA DDR: BRCA + PARPi Sapacitabine (nucleoside DDR: BRCA sapacitabine + seliciclib Worldwide (except Japan) analogue) AML Data Analy sis CYC140 (PLK1 inhibitor) Solid + blood cancers IND-ready PhI FIH Worldwide CYC202 Cushings disease, RA, cy stic f ibrosis Investigator sponsored CYC065: MYCN CYC065 Nueroblastoma trials CYC065 MCL-1 CYC065 MLL-r leukemias Source: Company Documents (2018)

ROLE OF MCL-1 EXPRESSION IN HEMATOLOGIC MALIGNANCIES

Mcl-1 is a Bcl-2 family member known to regulate cell survival in a range of hematologic malignancies including AML and CLL. Increased Mcl-1 protein expression has been associated with increased cell survival and downregulation of apoptotic activity. Several preclinical studies have suggested inhibition of CDK7 and CDK9 results in suppression of Mcl-1 transcriptional activity in patients with certain hematologic malignancies. This mechanism of Mcl-1 inhibition appears to be applicable independent of genetic profile including 17p status and Bim expression.

Mcl-1 is an anti-apoptotic protein regulating survival in multiple cell lineages. As such, directly shutting down Mcl-1 is unlikely to be feasible due to adverse events and short half- life of the protein. However, indirectly regulating Mcl-1 expression appears to offer varying levels of Mcl-1 regulation based at least in part on tumor histology.

Our Take: Current findings do not support a single strategy for regulating Mcl-1 across all histologies suggesting more than one potential pathway leading to Mcl-1 expression. As such, we view combination strategy as an important avenue for future development.

Furthermore, as a novel target with no approved therapies, in our view, there remains uncertainty regarding: 1) optimal level of Mcl-1 suppression; full suppression versus reduced suppression and 2) duration of inhibition; continuous dosing versus intermittent dosing. Preclinical studies from AstraZeneca (AZN, $37.07, Not Rated) and others have suggested intermittent dosing may offer clinically relevant Mcl-1 suppression with a better tolerability profile than continuous dosing. However, these findings have not been confirmed in clinical trials.

Our Take: Intermittent regulation of Mcl-1 is likely preferable to continuous dosing based on potential for better tolerability. As such, a broad Phase II program may be necessary to confirm dose schedule for all drugs in the class.

Page 6 Kevin DeGeeter 212.409.2027 Cyclacel Pharmaceuticals, Inc. (CYCC)

In terms of the development pathway for CDK-9 inhibitors in MCL-1 expressing cancers, most of the available literature focuses on AML and to a lesser extent CLL and other hematologic malignancies. The literature suggests potential synergy with both Bcl-1 inhibitors and PI3K inhibitors.

We believe a study published in the August 2013 issue of Blood entitled “Targeting acute myeloid leukemia by dual inhibition of PI3K signaling and Cdk9-mediated Mcl-1 transcription,” offers a clear overview of current thinking regarding the role of CDK-9 inhibition for treatment of hematologic malignancies. The authors noted targeting Bcl-2 or Bcl-x has shown promising activity against AML. However, AML cells are often dependent on Mcl-1 for proliferation, which can lead to reduced response to Bcl-targeted drugs. Furthermore, Mcl-1 amplification is linked to poor prognosis in AML. Through a series of stepwise experiments the authors demonstrated “targeting either Cdk9:Mcl-1 or PI3K:Bcl- xL alone is less effective at inducing apoptosis when compared with combined targeting in primary AML cells”.

OVERVIEW OF CDKS AND CELL CYCLE BIOLOGY

Uncontrolled cell division and proliferation, which are hallmarks of all cancers, are regulated through multiple steps collectively referred to as cell cycle biology. Each of the programs from CYCC’s product pipeline are based on internal research into the potential for targeting specific steps in cell cycle biology to treat cancer.

The human genome encodes 21 CDKs (1-11a, 11b-20) and over 15 cyclins (A-L, O, T, Y). Major cyclin-dependent kinases (CDKs) and cyclins involved in cell cycle regulation are 1, 2, 3, 4, and 6 and A, B, D, E, respectively. CDK 2, 4, and 6 along with cyclins D and E are involved in the regulation of cell cycle through the G1 phase. CDK 1, 2, 3 along with cyclins A, B, and E participate in the regulation of the S, G2, and M phases. CDK 7, 8, 9, and 11 along with cyclins C, H, L, and T are key players in transcription regulation/RNA processing.

Many of the first generation CDK inhibitors were subsequently recognized to be pan-CDK inhibitors with limited specificity for a particular CDK. Flavopiridol, which was assessed in over 60 clinical trials, inhibits CDK1, CDK2, CDK4, CDK6, CDK7 and CDK9. While demonstrating positive efficacy signals, the drug was not evaluated in Phase III development due to tolerability. Second generation CDK inhibitors such as dinaciclib maintained the pan-CDK profile but improved selectivity for specific CDKs. Specifically, dinaciclib demonstrated more potent inhibition of CDK1, CDK2, CDK5 and CDK9 (IC50 1- 4nM) while showing less potency for CDK6, CDK6 and CDK7 (IC50 60-100 nM).

Importantly, none of the earlier generations of pan-CDK inhibitors or the approved CDK4/6 inhibitors have validated biomarkers associated with clinical response. Preliminary work on resistance markers, including data on the CDK4-RB-p16 pathway, appears more promising. Specifically, preclinical studies have showed loss of RB and high expression of p16 are markers of resistance to CDK4/6 inhibition.

Our Take: Inhibiting transcription CDKs such as CDK7, CDK8 and CDK9 may be more amenable to biomarker strategies than CDK4/6 inhibitors due to ability to measure expression of downstream protein expression such as Mcl-1.

Cell cycle biology is grouped into four distinct phases: G1, S, G2, and M. Activation of each phase is dependent upon progression and completion of the preceding phase. Each phase is regulated by numerous interactions including intracellular factors and extracellular signaling. In general, potent inhibition of any one phase of the cell cycle leads to premature apoptosis. In clinical practice different cancer histologies tend to overexpress different transcription factors resulting in dysregulation of a specific phase of the cell cycle.

Page 7 Kevin DeGeeter 212.409.2027 Cyclacel Pharmaceuticals, Inc. (CYCC)

Figure 2. Overview of Cell Cycle Phases

Source: Khanh T. Do, AACR Annual Meeting 2018

CDKs promote succession through all phases of the cell cycle. CDK4, CDK6, CDK2 and CDK1 directly promote cell cycle progression and related impact on proliferation. CDK7, CDK8 and CDK9 are primarily associated with regulating transcription. CDK7 has been shown to have a general role in the phosphorylation of the RNA polymerase II (RNAPII) C- terminal domain that contributes to the initiation of transcription. CDK9 also phosphorylates RNAPII, thereby promoting elongation of transcription. Finally, CDK11 acts on the splicing machinery. In each of these contexts the CDK activity is directed by specific cyclin interactions.

CDK9 CDK9 is a subunit of the positive transcription elongation factor b (P-TEFb), also comprising CycT1 or CycT2, and is required for transcription elongation by RNAPII. CDK9 is responsible for the maintenance of antiapoptotic proteins such as Mcl-1, a Bcl-2 family member and a central regulator of cell survival and apoptosis. Transcriptional regulation is tightly controlled by CDK9 via phosphorylation of residues on the C-terminal domain (CTD) of RNAPII, which downregulates activity of suppressors that inhibit RNAPII activity. Inhibition of CDK9 mediated phosphorylation of the CTD RNAPII results in reduced levels of antiapoptotic proteins such as Mcl-1. Short-term CDK9 inhibition suppresses Mcl-1 transcription and rapidly depletes Mcl-1 protein (due to short half-life of the protein) resulting in caspase activation and cell death in Mcl1-dependent cancer cells.

CDK2 Many proteins involved in cell cycle progression are phosphorylated by CDK2, which is structurally and functionally related to CDK1. Proteins involved in cell cycle progression such as p27 and RB, DNA replication factors A and C, histone synthesis, and centrosome duplication are regulated by CDK2 through cyclin E and cyclin A to form active kinase complexes. CDK2 is regulated primarily through CDK-interacting protein/kinase inhibitory protein (CIP/KIP) and by the activity of RB and E2F. CYC065 has activity against CDK2 but the clinical relevance of the target may be secondary to CDK 9, in our view.

CDK4/6 As mentioned above, most of the approved CDK inhibitors regulate CDK4 and CDK6. These drugs regulate different biology than CYC065 and are not competitors, in our view. CDK4/6 activation promotes entry into the cell cycle and facilitates progression from G1 phase to S phase. Activity of CDK4 and CDK6 is linked to regulation of D-type cyclins, notably cyclin D1, cyclin D2 and cyclin D3. CDK4 and CDK6 activity is most closely associated with the tumor suppressor retinoblastoma protein (RB), CDK4 inhibitor proteins such as INK4 subtypes P16, and RB related proteins p107. Mutations in RB1 and deletions of CDK inhibitor genes such as CDKN2A can lead to uncontrolled cell cycle

Page 8 Kevin DeGeeter 212.409.2027 Cyclacel Pharmaceuticals, Inc. (CYCC)

initiation and subsequent proliferation. Regulating this group of CDKs has resulted in multiple therapies for treatment of HR+/HER2- advanced or metastatic breast cancer following endocrine therapy. As a class, the most clinically important adverse events associated with currently approved CDK4/6 inhibitors are Grade 3 and Grade 4 neutropenia. It is unclear if neutropenia is a class effect for all CDK inhibitors or is primarily related to regulation of CDK4/6, in our view.

Table 4. Approved CDK4/6 Inhibitors Developmental and Approved CDK Inhibitors Therapeutic Target Indication Regimen Approved Date Verzenio (Eli Lilly) CDK4/6 HR+, HER2- BC Mono;Combo w/ faslodex Feb 2018 Kisqali (Novartis) CDK4/6 HR+, HER2- BC Combo w/ letrozole Mar 2017 Ibrance (Pfizer) CDK4/6 ER+, HER2- BC Combo w/ letrozole Mar 2017 HER2- BC; anti- Mono;Combo w/ CYC065 (Cyclacel) CDK2/7/9 NA HER2 venetoclax or trastuzumab Source: Ladenburg Thalmann estimates

CYC065 – POTENTIAL 1ST-IN-CLASS CDK9 INHIBITION

CYC065 is a selective, second-generation ATP-competitive inhibitor of CDK2 and CDK9 designed to target Mcl-1 mediated apoptosis of cancer cells with lower levels of myelosuppression than earlier generations of CDK9 inhibitors. Additionally, the compound inhibits CDK2 expression, which is associated with cyclin-E expression and may offer a secondary mechanism of action. An intravenous formulation of the compound has completed Phase I development and CYCC is cautiously optimistic an oral formulation may be optimized in the next 12-24 months.

Dose limiting toxicities in Phase I included diarrhea, neutropenia and febrile neutropenia. Investigators indicated neutropenia was reversible without transfusions and the overall myelosuppression profile was better than with the first generation CDK9 inhibitor dinaciclib from Merck (MRK, $69.38, Not Rated). We do not view diarrhea, which was generally mild and reversible, as a limitation to future development either as monotherapy or combination therapy, and, in our view, anti-diarrheal prophylaxis may be adequate to relieve symptoms for most patients.

Our Take: The primary barrier to successful clinical development is likely myelosuppression and overall adverse event profile. As such, we view exploration of different dose levels and schedules in Phase II as important for successful development and as de-risking events for CYCC shares.

In terms of the competitive landscape, we would note CYC065 appears to be the only compound in clinical development regulating both CDK2 and CDK9. Specifically, in an article published in the January 2018 issue of Molecular Oncology entitled “Molecular profiling and combinatorial activity of CCT068127: a potent CDK2 and CDK9 inhibitor,” the authors concluded CDK2 expression may regulate CDK9 through a feedback loop, which suggests targeting both may be necessary for sustainable suppression of Mcl-1. If this hypothesis is borne out in clinical development, CYC065 may offer superior potency over selective regulation of only CDK9. Our base case assumes potency differences for molecules in the class will be driven primarily by level of CDK9 target engagement and compliance/tolerability of regimen.

CYC065 PRECLINICAL PROFILE: PROMISE FOR COMBOS

While the half-life of the CYC065 is 3 hours, the impact on Mcl-1 expression was observed for 24+ hours, which, in our view, suggests activity may be driven by AUC rather than cMAX. Furthermore, preclinical studies have demonstrated sustained inhibition of CDK9 is likely not required for Mcl-1 regulation and intermittent dosing may be appropriate. However, a review of the literature offers little agreement regarding a clinically important threshold for Mcl-1 expression. As such, we believe Mcl-1 is unlikely to be a useful biomarker for pharmacodynamic modeling for CDK 9 inhibitors.

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While we view target engagement as an imperfect proxy for pharmacodynamic activity, in general we would expect longer target engagement to offer greater flexibility in tailoring dose and schedule.

Our Take: Intermittent dosing appears to be preferable. However, the absence of a robust biomarker will require optimal dose schedule to be evaluated empirically.

Preclinical evidence suggests efficacy in CLL for CYC065 + venetoclax combination regimen.

Preclinical data presented at the 2018 AACR annual meeting supported efficacy of the combination regimen of CYC065 and venetoclax, a Bcl-2 inhibitor approved for patients with CLL including those with 17p deletions. Venetoclax demonstrated an IC50 of 0.07 µM while CYC065 had an IC50 of 0.8 µM shown in Figure 3.

Figure 3. Both CYC065 and Venetoclax have Single Agent Activity

The logic for combination therapy is based on parallel targeting of proteins crucial in CLL proliferation to elicit a more durable antitumor response that leads to apoptosis. CYC065 exhibited strong inhibition against CDK2/Cyclin E and CDK2/Cyclin A with IC50 of 3.5nM and 4.5nM, respectively. Table 5 below shows the inhibition profile towards various CDK family members implicated in CLL when CYC065 was dosed in combination. These results suggest that CYC065’s potency and selectivity are not hindered when used in such a combination regimen.

Table 5. Strong Activity Against CDK2 and CDK9 CYC065 CDK Inhibition Profile Kinase IC50, nM Cdk2/Cyclin E 3.5 Cdk2/Cyclin A 4.5 Cdk9/Cyclin T 26.2 Cdk5/p35 20.5 Cdk7/Cyclin H 193 Cdk4/Cyclin D 232 Cdk1/Cyclin B 578 Cdk6/Cyclin D >10,000 Source: AACR 2018; Abstract#5095

A time course study in cellular conditions mimicking the lymph node microenvironment demonstrated venetoclax reached a dose able to induce apoptosis within 6-8 hours and CYC065 was able to induce apoptosis after 24 hours, as shown in Figure 4 below. The onset of action is consistent with each drug’s mechanism of action and potential synergy.

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Figure 4. Evidence of Preclinical Synergy with Venetoclax

CLINICAL DEVELOPMENT OF CYC065 – ENTERING PHASE II

As mentioned above, we expect tolerability to be associated with dose schedule and formulation. Most of the CDK9 programs in clinical development, including CYC065, are being evaluated with a long 3-hour or 4-hour infusion. CYCC is currently evaluating CYC065 in a Phase I Part 2 study transitioning from a four-hour intravenous infusion once every 3 weeks to lower dose 2 days per week for 2 weeks of a 3-week cycle. We believe this dosing flexibility could be an important competitive advantage, particularly if patients need to reduce due to tolerability.

Separately, CYCC is working with third party contractors to optimize an oral formulation and hopes to begin bioequivalence studies in 2H18. We view an oral formulation as offering important potential differentiation from other CDK9 inhibitors and to be important for 1) combination studies with other oral therapies such as venetoclax tablets for hematologic malignancies and 2) potentially PARP inhibitors for ovarian cancer and breast cancer.

Our Take: Optimizing oral formulation in the next 12-24 months would offer important differentiation and be important in combination therapy with other oral targeted agents such as venetoclax.

AACR 2018 – Clear Mcl-1 Activity Results from the open label, dose escalation Phase I study were presented at the 2018 annual meeting of the American Association for Cancer Research (AACR). The study investigated CYC065’s effects on the Mcl-1 biomarker. In Part 1 of the study, prolonged suppression of Mcl-1 was observed in 11 out of 13 patients treated at the recommended Phase II dose, or RP2D, of 192 mg/m2/day following a single dose of CYC065. Preliminary anticancer activity was observed in 6 patients, of which 5 were treated at the RP2D and 3 of which were reported by investigators to have molecular features of their cancers associated with CYC065’s mechanism of action (overexpression or amplification of Mcl-1, MYC and/or cyclin E). The study is being conducted at the Dana Farber Cancer Institute in Boston. The findings suggest potential activity in adult and pediatric hematological malignancies including AML, Acute Lymphocytic Leukemias (ALL), CLL, B-cell lymphomas, multiple myeloma, and certain solid tumors, including uterine cancers and neuroblastomas.

CYC065 was studied in 26 heavily treated patients with advanced cancers who were infused with CYC065 over 4 hours every 21 days. The study enrolled seven dose levels ranging from 8 mg/m2 per day to 288 mg/m2 per day. Patient and disease characteristics are shown in Table 6.

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Table 6. Phase I Demographics

Phase I Patient + Disease Characteristics Age Median (range) 63 (43-71) 0 6 ECOG 1 20 Male 5 Gender Female 21 Ovarian (papillary, serous, transitional) 14 Uterine (carcinosarcoma, endometrial) 4 Histology HN (SCCHN, carcinoid, adenoid cyctic) 6 Pancreatic 1 CRC 1 Source: AACR 2018; Abstract#CT037 Adverse events were consistent with preclinical modeling with neutropenia levels in line with our expectations. Below we outline patient inclusion and DLT criteria.

Table 7. Overview of Phase I DLTs

Phase I Eligibility + DLT Criteria Key Inclusion Criteria DLT Toxicity Criteria - Advanced solid tumors progressed on standard therapies -Grade 3 or 4 non-hematological toxcicity (except alopecia, or have no effective therapy inadequately treated nausea, vomiting, diarrhea) -ECOG PS 0-1 -Grade 3 or 4 AST/ALT w/ Grade 2 elevation of bilirubin -Evaluable disease -Neutropenic fever/ Grade 4 neutropenia >5 days -Adequate organ function: -Grade 4 thrombocytopenia/ Grade 3 thrombocytopenia -Absolute neutrophil count ≥1.5x109/L associated w/ bleeding platelets ≥100x109/L -Grade 4 anemia -Total bilirubin ≤1.5xULN, ALT ≤1.5xULN -Treatment delay >2 weeks due to drug-related AEs -Creatinine ≤1.5xULN or creatinine clearance >60 mL/min Key Exclusion Criteria: MTD: highest dose level at which less than 2/6 patients - Untreated CNS metastases or evidence of CNS experience DLT in cycle 1. progression on MRI w/in 4 wks prior to enrollment for treated RP2D: dose at which less than 1/3rd of patients experience CNS metasteses a DLT during cycle 1 in a confirmatory expansion cohort Source: AACR 2018; Abstract#CT037 The primary outcome measure was the number of patients experiencing DLTs in cycle 1, the standard methodology for determining MTD and the RP2D. Clinical response was reported in patients with Mcl-1 amplified (ovarian cancer, parotid acinic cell carcinoma), MYC amplified (uterine carcinosarcoma, ovarian cancer) and cyclin E amplified (ovarian cancer) tumors. Investigators also sought to evaluate PK and assess PD markers such as RNAPII CTD-Ser2 and Mcl-1 levels. RP2D of 192mg/m2 was selected partly based on the DLT profile of 13 patients shown in Table 8. At the highest dose patients experienced reversible neutropenia, febrile neutropenia and diarrhea.

Table 8. Myelosuppression Drives DLTs CYC065 Phase I DLT Profile in Solid Tumors Dose mg/m2 Number of patients DLTs 8 1 - 16 2 - 32 2 - 64 3 - 128 4 - n=1: Grade 3 diarrhea n=1: Grade 3 diarrhea w/ hypomagnesemia Grade 3 febrile neutropenia 192 13 Grade 3 hypocalcemia w/ WBC lysis (RP2D) ALT, AST, bilirubin elevations Grade 4 leukopenia + thrombocytopenia Grade 3 mucositis + dehydration 288 1 n=1: Grade 4 neutropenia, Grade 3 febrile neutropenia Source: AACR 2018; Abstract#CT037

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CYC065 showed a relatively short half-life between 1.6-3.9 hours. At the RP2D, 11 of 13 (85%) patients experienced consistent suppression in Mcl-1 lasting for at least 24-hours, which in our view, represents durable target suppression after a single dose of 192 mg/m2.

Table 9. High Levels of Mcl-1 Suppression at Phase II Dose

Phase I Pharmacodynamic Analysis Dose mg/m2 Patients Decrease in Mcl-1 at 24 hours 8 1 0 16 2 0 32 2 1 64 3 1 128 4 2 192 13 11 288 1 1 Source: AACR 2018; Abstract#CT037 The data included pharmacodynamic analysis of response to treatment with CYC065 for one patient, Patient 14. At the RP2D and after 24 hours of treatment, RNAPII CTD Serine 2 residue was not phosphorylated in Patient 14, as assessed by Western Blot analysis using an antibody that binds only to phosphorylated Ser2 residues on RNAPII, suggesting that elongation was inhibited through CDK9 inhibition. This patient concurrently exhibited undetectable levels of Mcl-1, suggesting CYC065 can sustain durable inhibition of CDK9 as well as Mcl-1. Furthermore, as an indicator of apoptosis, PARP cleavage was observed in this patient beginning 4-hours post dosing and continuing another 8 hours, after which undetectable levels were observed.

Part 2 of the Phase I study is slated to enroll patients who present advanced cancers to evaluate efficacy in Mcl-1, MYC and cyclin E amplified cancers.

Neuroblastoma The American Cancer Society estimates roughly 800 neuroblastoma patients are diagnosed each year in the U.S. with 90% of cases diagnosed by age 5 years. The literature suggests 40-50% of these patients have MYC-M amplification. CYCC is exploring opportunities to work with a clinical trials consortium with specialty in pediatric neuroblastoma to evaluate the role of CYC065 IV in pediatric neuroblastoma in patients with MYC-M overexpression. Preclinical studies suggest MYC-M overexpression may be mutually exclusive from TRK gene fusions. As such, this patient population represents a significant unmet medical need. Management estimates roughly half of patients have MYC-M amplification.

The clinical trial network accesses around 50 patients a year. Enrollment of a Phase I dose escalation study and small expansion cohort could take around 12 months, in our view. Initiation of the study is 3-6 month behind the CLL combination study, according to management, which suggests potential to begin the study before the end of 2018. A manuscript describing the preclinical data has been submitted for publication.

BCL-2 AND BTK INHIBITORS GAIN GROUND IN CLL

Until five years ago chemotherapy in combination with CD20 agents was the primary treatment option for most CLL patients, both in frontline setting and for relapsed/refractory disease. With the growing acceptance of BTK inhibitors such as ibrutinib in the frontline setting and potential of the BCL-2 inhibitor venetoclax to be established as the standard of care in second line setting, we believe 1) chemotherapy will be less relevant to treatment of CLL, at least in the U.S., and 2) combination regimens of two or more targeted agents may offer higher complete response rate effectively “curing” more frontline patients and providing more durable responses in the second line setting.

Most CLL patients in the U.S. are treated in the frontline setting with either ibrutinib BTK inhibitor monotherapy or chemotherapy with or without Rituxan. Current trends suggest

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BTK inhibitors are likely to become the dominant treatment based on potential to avoid the side effects of chemotherapy in an older population (average age of diagnosis for CLL is 70 years). A review in the May 2018 issue of Blood noted 5-year PFS for treatment naïve CLL patients receiving ibrutinib was 74.4%. BTK inhibitors are less active in relapsed/refractory patients (5-year PFS was 19.4% for relapse/refractory patients in the same study).

For patients progressing on a BTK inhibitor, we believe most hematologists in the U.S. seeking to use targeted therapies will prescribe either the BCL-2 inhibitor venetoclax or the PI3K inhibitor idelalisib. Anti-CD20 agents such as Rituxan are also used in some patients.

Our Take: Based on available data we expect venetoclax to emerge as the preferred 2nd- line agent for treatment of CLL based on data demonstrating healthy responses in patients failing prior treatment with the BTK inhibitor ibrutinib.

Our outlook assumes chemotherapy regimens are used primarily in the frontline setting to achieve deep remissions but do expect some patients to be offered chemotherapy in the 2nd line setting. Multiple studies have demonstrated CLL patient with 17P deletions have a less robust response to chemotherapy. As such, at the margin we would expect CYC065 and other target CDK9 inhibitors to be used more frequently in patients with 17P deletions based on the more limited benefit of chemotherapy as an alternative treatment.

In terms of potential expansion into frontline treatment for CLL, in our view, there remains an unmet need in offering deeper remission for BTK-treated patients to support patients going off drug for extended periods – currently most patients must remain on BTK therapy until disease progression. Exploring combinations of a BTK inhibitor with a short course of therapy with a BCL-2 inhibitor such as venetoclax or CDK9 inhibitor such as CYC065 to drive more patients to a complete response may be an area for future clinical trials, in our view.

CDK9 COMPETITIVE LANDSCAPE

While CYC065 regulates both CDK9 and CDK2, our analysis of the competitive landscape focuses on inhibition of CDK9 as the most plausible mechanism for a differentiated clinical profile. As mentioned above, in our view, the primary clinical relevance of CDK9 inhibition in oncology is as a strategy for regulating MCL-1. As such, we do not view approved CDK inhibitors, including the widely used CDK 4/6 inhibitors, as competitive with CYC065 or other CDK9 inhibitors. Lastly, we expect CDK9 inhibitors to potentially be used in combination with other drugs including venetoclax. As such, we review the performance profile of venetoclax to assess the baseline performance of monotherapy.

While pan-CDK inhibitors such as AT7519 from Cancer Research UK and Dinaciclib from Merck do hit CDK9, we believe the lack of specificity limits potency and do not include the compounds in our analysis. Preclinical data suggests BAY 1143572 from Bayer (BAYRY, $21.96, Not Rated) is selective for CDK9 but there is limited public data about the compound’s profile or development status. Eli Lilly’s (LLY, $105.37, Not Rated) LY2857785 is described as a CDK9 inhibitor but the last public update we are aware of was in 2014.

Alvocidib The IV CDK9 inhibitor was discovered by Tolero Pharmaceuticals and was acquired in 2017 by Sumitomo Dainippon Pharma.

Our Take: Alvocidib is potentially a first-to-market CDK9 inhibitor and a direct competitor for CYC065. We believe CYC065 is differentiated based on potential for both IV and oral dosing compared to IV dosing with alvocidib, potential for better tolerability and different paths to regulatory approval in AML (alvocidib) and CLL (CYC065). The role of CDK2 inhibition with CYC065 may also be important.

In June 2018 at the European Hematology Association meeting Tolero presented positive data from Stage 1 of the Phase II program for alvocidib, including complete remission

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(CR) or complete remission with incomplete recovery (CRi) rate of 61% (11/18 patients). Median duration of response was 8.2 months. Among 11 patients with refractory disease, 8 achieved CR or CRi. Five of these patients went on to receive stem cell transplant.

All patients were dosed with: 1) IV alvocidib at a dose of 30mg/m2 delivered over 30 minutes followed by 60 mg/m2 IV over 4 hours administered daily for the first 3 days of a treatment cycle, 2) cytarabine 2 gm/m2 by continuous IV over 72 hours on days 6-8 and with 3) mitoxantrone 40mg/m2 IV over 1-2 hours, starting 12 hours after completing cytarabine to be administered on day 9 of the 10 day cycle.

A total of 176 AML patients were screened to enroll 21 patients with Mcl-1 dependent cancer. MCL-1 dependence was measured by mitochondrial BH3 profiling, which we do not view as a well validated screening technique and may confound the results.

Roughly 52% (11 of 21) of patients enrolled were refractory AML, 19% (4/21) were early relapse and, 29% (6/21) were late relapse. A total of 18 patients completed all follow up. Three patients died while on study (2 from sepsis and 1 from mitral valve replacement).

Grade 3 or greater adverse events included tumor lysis syndrome, sepsis, diarrhea, and elevated AST. While these toxicities are all associated with cytarabine and mitoxantrone therapy, in our view, the 2 deaths associated with sepsis is a cause for concern regarding myelosuppression.

Based on results from the first 21 patients, Sumitomo has opened Stage 2 of the study with AML patients randomized to receive either alvocidib in combination with cytarabine and mitoxantrone or cytarabine and mitoxantrone alone. The study, which will have a primary endpoint of complete remission, is expected to enroll 106 patients.

AZD4573 The IV CDK9 inhibitor is currently in Phase I development at AstraZeneca in patients with relapsed or refractory hematologic malignancies. AstraZeneca has not disclosed interim efficacy data from the open label study. Expected completion date for the Phase I program is October 2019, according to clinincaltrials.gov.

Our Take: Broad AZD4573 Phase I program in nearly all common hematologic malignancies including multiple myeloma CML, and ALL should offer valuable insight into potential breadth of addressable markets for selective CDK9 inhibitors.

In terms of the Phase I study design, 42 patients will be randomized into 2 arms with six cohorts in each arm. Arm A will dose subjects with relapse/refractory hematological malignancies while Arm B will dose subjects with relapse/refractory AML, ALL, high-risk MDS, CMML, CLL and Richter’s syndrome.

Eligible patients will have 1) histologically confirmed relapse/refractory patients who have received at least 2 prior lines of therapy, 2) documented active disease by NCCN or ESMO guidelines, 3) adequate hematologic, hepatic, and renal function and 4) ECOG performance status of ≤2.

In terms of preclinical data, AstraZeneca presented a poster at the 2018 AACR meeting demonstrating anti-cancer activity across different hematological malignancies including AML, NHL, CLL, and multiple myeloma. AZD4573 also demonstrated activity in combination with the BTK inhibitor acalabrutinib, which we view as important for potential expansion into the frontline treatment settings. AZD4573 was a potent inhibitor of CDK9 (IC50 of <0.004 μM) with short half-life of 16 minutes. Short-term treatment with AZD4573 led to a rapid dose-dependent and time-dependent decreases in cellular pSer2-RNAPII, resulting in activation of caspase 3 and cell apoptosis.

Venetoclax Oral Regimen for CLL The lead indication for CYC065 is a combination regimen with the BCL-2 inhibitor venetoclax for patients with relapse and refractory CLL. In June 2018, FDA approved venetoclax for 2nd line CLL patients and small lymphocytic lymphoma (SLL) patients with or without 17p deletion. The approval marks one of the first treatment regimens for CLL

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that spares patients the toxicity of chemotherapy, which, in our view, could drive standard of care toward oral treatments and potential combination regimens such as CYC065.

Our Take: Recent FDA approval should drive venetoclax toward becoming standard of care in 2nd line CLL, which increases the clinical significance of development for CYC065 in combination with venetoclax.

Venetoclax was approved based on results from the 389-patient open-label MURANO study demonstrating venetoclax plus rituxan was superior to bendamustine plus rituximab. Patients received 5-week lead in dosing of venetoclax followed by 400 mg once daily of venetoclax for 24 months. Patients received 6 cycles of Rituxan at 375 mg/m2 for cycle 1 and 500 mg/m2 at the beginning of the next five 28-day cycles. Subjects in the bendamustine plus rituximab cohort received 6 cycles of 70 mg/m2 of bendamustine on days 1 and 2 of each cycle with the same dosing regimen of rituxan as the venetoclax cohort.

Table 10. Response Rates for Venetoclax in CLL Investigator-assessed Best Overall Response Rates for MURANO Study Venetoclax + rituximab Bendamustine + rituximab Difference P-value Overall Response 181/194 (93.3%) 132/195 (67.7%) 25.6% (17.9-33.3) p<0.0001b CR/CRia 52/194 (26.8%) 16/195 (8.2%) 18.6% p<0.0001b PR/nPR 129/194 (66.5%) 116/195 (59.5%) Stable disease 4/194 (2.1%) 44/195 (22.6%) Progressive disease 3/194 (1.5%) 6/195 (3.1%) Missing/unavailable 6/194 (3.1%) 13/195 (6.7%) aCR confirmed by bone marrow assessment and CT scan; b Descriptive p-value Source: Blood. 2017 Dec 130:LBA-2.

The primary endpoint was progression-free survival (PFS). At the median follow-up of 23 months, PFS in the bendamustine cohort was 18.1 months while PFS for the venetoclax cohort had not been met. ORR was 72% in the bendamustine cohort compared to 92% in the venetoclax cohort.

Table 11. Safety Profile of Venetoclax in CLL Phase III MURANO Adverse Events Venetoclax-Rituximab Bendamustine-Rituximab (N=194) (N=188) Grade 3 or 4 AE - no. pats. (%) 159 (82.0) 132 (70.2) Total no. of events 335 255 Grade 3 or 4 AE ≥ 2% diff 130 (67.0) 104 (55.3) incidence b/n groups - no. pats. 112 (57.7) 73 (38.8) Neutropenia Febrile neutropenia 7 (3.6) 18 (9.6) SAE ≥ 2% incidence in either 90 (46.4) 81 (43.1) group - no. pats. (%) Febrile neutropenia 7 (3.6) 16 (8.5) Fatal AE no. pats. (%) 10 (5.2) 11 (5.9) Source: N Engl J Med. 2018 Mar 22;378(12):1107-1120.

Notable Grade 3 adverse events with venetoclax treatment included neutropenia, diarrhea, upper respiratory tract infection, fatigue, cough, and nausea. About 31% of patients had Grade 4 neutropenia. Serious infections occurred in 21% of patients with pneumonia (9%) being the most common infection. Additionally, tumor lysis syndrome was reported, which requires active surveillance and patient management for clinicians. Given reports of tumor lysis syndrome in Phase II development with the CDK9 inhibitor alvocidib, in our view, this is an area of potential overlapping toxicity in combination therapy for CYC065 and venetoclax.

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Table 12. Safety Profile of Venetoclax in CLL Summary of AEs for Venetoclax Adverse Events Venetoclax + rituximab Bendamustine + rituximab Number of AEs 335 255 Grade 3-4 AEs occurring ≥5% pts in either arm, n(%) Neutropenia 112 (57.7) 73 (38.8) Anemia 21 (10.8) 26 (13.8) Thrombocytopenia 11 (5.7) 19 (10.1) Febrile neutropenia 7 (3.6) 18 (9.6) Pneumonia 10 (5.2) 15 (8.0) Infusion-related reaction 3 (1.5) 10 (5.3) Serious AEs in ≥2 pts in either arm, n(%) Pneumonia 16 (8.2) 15 (8.0) Influenza 3 (1.5) 2 (1.1) Sepsis 1 (0.5) 4 (2.1) Upper respiratory tract infection 3 (1.5) 2 (1.1) Lung infection 3 (1.5) 0 Sinusitis 2 (1.0) 1 (0.5) Appendicitis 2 (1.0) 0 Bronchitis 0 2 (1.1) Pharyngitis 0 2 (1.1) Respiratory tract infection 2 (1.0) 0 Fatal AEs, n(%) 10 (5.2) 11 (5.9) AE reporting period: up to 90 days after end of bendamustine treatment (6mo max); up to 28 days after end of venetoclax treatment (2yr max). Source: Blood. 2017 Dec 130:LBA-2.

CYC065 REVENUE MODEL - $650M IN PEAK SALES

Our CYC065 revenue forecast focuses on relapsed/refractory CLL based on 1) significant unmet need with median survival in refractory population of less than two years, 2) potential to combine with other targeted agents such as BCL-2 inhibitors and 3) good treatment options currently available in the frontline setting. Our model segments revenues by U.S. and ROW with the U.S. market representing 80%+ of the market opportunity based on a clear regulatory and reimbursement path for targeted cancer therapies.

About 60,300 Americans are diagnosed with leukemia each year, according to the American Cancer Society. Roughly 30% to 35% of leukemia patients are diagnosed with CLL for annual incidence rate of 20,940.

As mentioned above, prognosis for frontline treatment is good for most patients with recent studies suggesting a 5-year PFS rate approaching 75% with the BTK inhibitor ibrutinib. Furthermore, data from the SEER database suggests a 5-year survival greater than 84%. However, complete response rates are only about 20% and roughly 80% of patients develop refractory or relapsed disease, which suggests an addressable market of roughly 16,800 patients.

While we believe there will likely be market segmentation by genetic profile such as 17P deletion status, in our view, available data does not adequately describe which genetic features will be most relevant when treating with a CDK9 inhibitor. As such, we do not segment the market by genetic profile.

Our model calls for CYC065 to capture 23% of the target U.S. relapsed/refractory CLL market in 2025 (last year of DCF model) and 30% by 2027 based on growing acceptance of BCL-2 targeted agents in the second-line setting. We expect CYC065 to be priced at about $150,000 annually, or $12,500 per one-month treatment cycle in the U.S., which is similar to other hematologic cancer salvage therapies.

Our model assumes CYC065 is dosed continuously until disease progression. In the absence of clinical data for CYC065 the duration of response is difficult to forecast but we view 7 cycles of therapy as a reasonable minimum threshold for a commercially viable drug, which implies around $87,500 per patient.

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We expect the company to eventually partner CYC065 for ROW, in exchange for economics equivalent to 13%-18% royalty on net sales (point estimate of 15%). As a methodological point, we do not include partner milestones in our revenue model due to limited visibility on timing and capture milestone economics through a higher royalty rate on future sales.

We expect CYC065 to be launched in the U.S. during 2023 and outside the U.S. in 2024. On net, our forecast translates to revenue to CYCC of $381.2M in 2025 including U.S. sales of $374.8M and international royalties of $6.3M on gross sales of $42.1M. We forecast peak sales in 2027 of $540.9M on a reported basis including $526M in U.S. sales, $99.6M from international markets and international royalties of $14.9M.

Table 13. CYC065 Revenue Model

CYC065 Revenue Model (in $millions) 2018E 2019E 2020E 2021E 2022E 2023E 2024E 2025E 2026E 2027E

U.S. CLL Market Model Americans Diagnosed with Leukemia (A) 60,300 - Projected Growth in Leukemia Population NA 0.7% 0.7% 0.7% 0.7% 0.7% 0.7% 0.7% 0.7% 0.7% Projected Number of U.S. Leukemia Patients 60,722 61,147 61,575 62,006 62,440 62,877 63,317 63,761 64,207

- % of U.S. Leukemia Patients - CLL Subtype (A) 35% 35% 35% 35% 35% 35% 35% 35% 35% 35% U.S. CLL Patient Population 20,900 21,046 21,194 21,342 21,491 21,642 21,793 21,946 22,099 22,254

- % of CLL Refractory / Relapse Setting 80% 80% 80% 80% 80% 80% 80% 80% 80% 80% CLL Patients Refractory / Relapse 16,720 16,837 16,955 17,074 17,193 17,313 17,435 17,557 17,680 17,803

% of 2nd Line CLL Population Receiving CYC065 0.0% 0.0% 0.0% 0.0% 0.0% 4.6% 13.9% 23.0% 29.3% 30.0% Number of Patients Treated 0 0 0 0 0 801 2,419 4,038 5,171 5,341 Number of Scripts per Patient 7.0 7.0 7.0 7.0 7.0 7.0 7.0 7.0 7.0 7.0 Total CYC065 Scripts 0.0 0.0 0.0 0.0 0.0 5,605 16,933 28,266 36,199 37,387 Price per Script $12,500 $12,500 $12,500 $12,500 $12,500 $12,500 $12,875 $13,261 $13,659 $14,069 Annual Treatment Cost $150,000 $150,000 $150,000 $150,000 $150,000 $150,000 $154,500 $159,135 $163,909 $168,826 Average Cost per Patient $87,500 $87,500 $87,500 $87,500 $87,500 $87,500 $90,125 $92,829 $95,614 $98,482 Increase in Price per Script 0.0% 0.0% 0.0% 0.0% 0.0% 0.0% 3.0% 3.0% 3.0% 3.0% U.S. Sales of CYC065 for r/r CLL ($M) $0.0 $0.0 $0.0 $0.0 $0.0 $70.1 $218.0 $374.8 $494.4 $526.0

CYC065 ROW Gross Revenues ($M) $0.0 $0.0 $0.0 $0.0 $0.0 $0.0 $18.0 $42.1 $68.2 $99.6 - Growth in ROW Revenues NA NA NA NA NA NA NA NA 61.9% 46.1%

Economics to CYCC 15% 15% 15% 15% 15% 15% 15% 15% 15% 15%

ROW Sales of CYC065 to CYCC ($M) $0.0 $0.0 $0.0 $0.0 $0.0 $0.0 $2.7 $6.3 $10.2 $14.9

Worldwide CYC065 Revenue to CYCC ($M) $0.0 $0.0 $0.0 $0.0 $0.0 $70.1 $220.7 $381.2 $504.7 $540.9 Source: Ladenburg estimates (A) American Cancer Society Estimates CYC140 – UNVALIDATED PLK1 TARGET OFFERS UPSIDE

CYC140 is a small molecule inhibitor of polo-like kinase-1 (PLK1), which is believed to regulate mitotic events during cell division, including microtubule rearrangement. We currently do not have any economics for the program in our financial model but will revisit our assumptions following release of Phase Ib/II from a competing PLK1 inhibitor, PCM- 075 from Trovagene (TROV, $0.81, Not Rated), in 2019.

Overexpression of PLK1 is observed in a range of hematologic malignancies and certain solid tumors (ovarian, NSCLC and urothelial). High expression of PLK1 has been associated with poor response to chemotherapy regimens including doxorubicin, paclitaxel and gemcitabine. However, evidence supporting inhibition of PLK1 as an important therapeutic target is mixed, in our view.

The PLK1 inhibitor volasertib demonstrated preliminary activity in a Phase II study of AML patients but failed in a Phase III study in combination with low dose cytarabine due at least in part to tolerability problems including elevated risk of infection, diarrhea and myelosuppression. Furthermore, a study published in the July 2017 issue of Nature Medicine presented data suggesting extended PLK1 inhibition may be associated with hypertension, blood vessel rupture and other cardiovascular toxicities in a mouse model.

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Our Take: Targeting PLK1 has demonstrated signs of anti-tumor activity in hematologic malignancies but the narrow therapeutic window and adverse event profile of first- generation therapies raises questions regarding viability of the target.

CYC140 and other second-generation PLK1 inhibitors seek to improve the tolerability profile through limiting off-target binding with PLK2 and PLK3 and by providing improved pharmacologic activity (i.e., shorter half-life to limit risk of drug accumulation and better PK profile).

Our Take: Trovagene’s PCM-075 appears to be a more selective PLK1 inhibitor than volasertib and Phase Ib/II data in 2019 offers the next opportunity to validate PLK1 as a target. We would view positive PCM-075 data as good for CYC140 by validating the potential for selective PLK1 inhibition.

CYCC is completing IND-enabling preclinical development of CYC140 with the support of a $3.5M grant from the Biomedical Catalyst of the United Kingdom and has disclosed plans to submit an IND for the compound during 2018. Based on this timeline we believe CYCC is well positioned to evaluate findings from the PCM-075 Phase Ib/II study to either accelerate clinical development or de-prioritize the program if the PCM-075 data is negative.

Preclinical Data Suggests Potential Development for Esophageal Cancer

CYCC presented data at the 2017 AACR meeting demonstrating synergy for CYC140 in combination with EGFR inhibitors and PI3K inhibitors, which supports the potential of an all-oral regimens for treatment of esophageal cancer. Specifically, the study evaluated roughly 250 cancer cell lines, including 15 esophageal cancer cell lines. CYC140 cellular IC50 correlated with induction of apoptosis in esophageal cancer cell lines while non- malignant cell lines demonstrated only transient inhibition of cell cycle activity. Importantly, xenograft data supported potential synergy with both chemotherapy agents such as cisplatin and irinotecan and targeted agents such as EGFR inhibitors, HDAC inhibitors and PI3K inhibitors.

SAPACITABINE – CLEAN FAILURE IN AML; LOOK TO PARPS

Sapacitabine is an oral prodrug for the nucleoside analog CNDAC that failed to meet the primary endpoint in Phase III development in combination with decitabine for newly diagnosed elderly AML patients. The rationale for development was based on 1) a 45% overall response rate (ORR) and 27% one-year survival in Phase II development at the recommended Phase III dose of 400mg, 2) significant unmet need for new treatment options to treat frail elderly AML patients and 3) relatively benign adverse event profile. In February 2017, the Phase III SEAMLESS study did not meet its primary endpoint of improvement in overall survival. In a prespecified subgroup of patients with low baseline peripheral white blood cell count (roughly two-thirds of the study’s population), sapacitabine did demonstrate an improvement in survival.

Our Take: While we believe sapacitabine may be an interesting agent to explore in future combination studies with other oral DNA damaging agents such as PARP inhibitors, continued internal investment by CYCC is not justified.

Like other nucleoside analogs, sapacitabine appears to regulate cell cycle arrest through inhibition of DNA replication. However, preclinical data suggests sapacitabine results in single-strand DNA damage during the S phase with excision to double-strand breaks during homologous recombination repair pathway common in many cancer cells. Most other nucleoside analogs work through the G2 pathway. This differentiated mechanism of action resulted in a more favorable tolerability profile, in our view.

Overview of SEAMLESS Data

SEAMLESS was a randomized Phase III study of sapacitabine as a front-line treatment in 482 elderly patients aged 70 years or older with newly diagnosed AML who were not candidates for intensive induction chemotherapy. All patients received a decitabine dose

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of 20 mg/m2 for 5 days every 4 weeks. Patients in the study drug arm also received sapacitabine 300mg bid for 3 consecutive days every 2 weeks.

On the primary efficacy endpoint of overall survival the sapacitabine arm demonstrated 5.9 month overall survival compared to 5.7 months in the control arm. Furthermore, one- year survival was comparable at 34% in sapacitabine-treated patients and 35% in the control arm.

Management noted there was a statistically significant improvement in survival based on the pre-specific subgroup analysis of white blood cell (WBC) count greater than 10,000 with sapacitabine-treated patients with low WBC recording survival of 8.0 months compared to 3.8 months for the high WBC subgroup. However, we are skeptical of the robustness of this finding. Specifically, in the control arm treated with only decitabine the high WBC patients had survival of 5.5 months compared to 3.8 months for patients treated with decitabine and sapacitabine (i.e., the addition of sapacitabine resulted in 2.3 month reduction in survival).

Our Take: In the absence of a plausible mechanism of action of why high WBC and sapacitabine treatment results in shorter survival than decitabine alone, we view the unexpectedly low survival in sapacitabine-treated patients with high WBC as a statistical outlier driving the apparent benefit of low WBC status and sapacitabine treatment.

Table 14. WBC Data Offers Signal but May be Outlier Survival Subgroup Analysis-Phase III SEAMLESS Study in elderly AML Sapacitabine/Decitabine Decitabine p-value Patients Median in months Patients Median in months WBC <10,000 145/157 8.0 146/162 5.8 0.145 WBC≥ 10,000 81/84 3.8 72/79 5.5 0.007 Source: Company documents; ASH 2017

COLLABORATION AND LICENSE AGREEMENTS We expect CYCC to eventually seek commercial development partners for each of its pipeline programs to support registration of the products in the EMEA and other countries outside of the U.S. We would note the company’s core asset – CYC065 – is currently unpartnered for all geographies. Below we detail collaborations funding the company’s non-core programs. We do not include any economics for these partnerships in our financial forecast for CYCC.

Seliciclib In June 2015, CYCC entered a collaboration agreement with ManRos Therapeutics SA to develop seliciclib capsules for the treatment of cystic fibrosis (CF). In 4Q17, CYCC received a $150,000 payment from ManRos and expects to receive an additional payment in 2018 related to a clinical development milestone. The company is also entitled to undisclosed royalties from future commercial sales of seliciclib for the treatment of CF. We do not include any economics for this agreement in our financial projections.

Seliciclib (also known as roscovitine) is a first-generation oral CDK inhibitor with activity against CDK2, CDK7, and CDK9. The ongoing 36-patient Phase II study is enrolling CF patients harboring at least 2 CF gene variants, including at least one F508del-CFTR mutation, and with a history of chronic pseudomonas infections. The 28-day study will evaluate 3 treatment dose regimens with data expected in 2H18, according to clinicaltrials.gov. The study is primarily designed to assess safety and PK profile.

Our Take: Short 28-day follow up in Phase II seliciclib study will provide limited efficacy data in CF patients. While we expect data in 2H18, we do not view the results as a material catalyst for CYCC shares.

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INTELLECTUAL PROPERTY

We believe CYCC is building a healthy intellectual property portfolio surrounding CYC065, including composition of matter patents valid at least through 2031. In total, CYCC has 25 U.S. patents, 14 patents granted by the European Patent Office and 59 granted patents in other countries. Additionally, the company has licensed 48 granted patents, has one patent application pending in the United States, and 18 patent applications pending in other countries.

CYCC has issued composition of matter patents relating to CYC065 in the United States and most other developed economies. The primary patent protection for the U.S. market is #8,889,861 entitled “crystalline forms of a purine derivative.” The company also has issued patents pertaining to use in combination with CDK inhibitors for treatment of proliferative disorders, which may offer extended patent protection depending on the course of future commercialization for CYC065.

Sapacitabine is protected by composition of matter patents for the U.S. into 2022, excluding patent extensions. In September 2003, CYCC licensed patents from Daiichi Sankyo describing the composition and use of sapacitabine and CNDAC. Daiichi Sankyo retains a right of first refusal to development rights for sapacitabine in Japan and is entitled to certain undisclosed royalties from future sales.

For CYC140, the company’s granted patent protection should extend at least through 2028, in our view.

MANUFACTURING AND SUPPLY

CYCC uses third-party CMOs to manage process development, production of active drug substance and fill-finish activities necessary to supply CYC065 and CYC140 to clinical trials. CYC065 is initially being developed in an IV formulation. Management recently reiterated plans to unveil a small molecule formulation of CYC065 in 2H18 to support development for extended dosing regimens to treat breast cancer and other solid tumors with elevated levels of cyclin E. While CYCC has not disclosed the third parties working on the oral formulation of CYC065, in our view, production will likely require a different supply chain than the IV formulation. Lastly, we do not believe the small molecule chemistry of CYC140 requires specialized API or excipients and, in our view, timely qualification of new suppliers should be feasible.

We would note CYCC does not disclose its third party CMOs and we cannot independently verify whether any of the CMO facilities have 483 warning letters or other compliance deficiencies that may impact regulatory review of the supply chain.

CAPITAL STRUCTURE AND SHAREHOLDER CONCENTRATION

Common stock in Cyclacel is traded on the NASDAQ Capital Market under the ticker ‘CYCC’. Prior to completing a reverse merger into Xcyte Therapies in March 2006, the predecessor company (Xcyte) traded on the NASDAQ under the ticker ‘XCYT’. As of June 30, 2018, CYCC had approximately 12.0 million common shares outstanding. Additionally, there were 7.5 million warrants outstanding with a strike price of $2.00 and nearly 800,000 management options (average strike price of $7.28).

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Table 15. Overview of Warrants, Options and Preferred Stock Option and Warrants Security Amount Stock Options** 796,856 Convertible preferred stock 1,698 Series A preferred stock 132,000 Warrants* 7,490,500 Total shares excluded from calculation 8,421,055 * Strike on warrant is $2.00; **Avg strike on options is $7.28 Source: Company reports

CYCC has a limited institutional shareholder base with 3 institutional investors and 2 insiders controlling approximately 24% of CYCC common stock. As of April 15, 2018, Eastern Capital was the only dominant shareholder with an 18% stake in the company.

Our Take: The current shareholder structure represents limited institutional investor awareness of the CYC065 story and residual impact from the negative Phase III sapacitabine study results in February 2017.

Table 16. Eastern Capital Controls 18% of Voting Stock Shareholder Structure Holder Shares % of Total Outstanding* Eastern Capital LTD 2,167,261 18.1% Vanguard Group 374,155 3.1% Spiro Rombotis 63,590 0.5% Virtu Americas LLC 39,613 0.3% Paul McBarron 35,055 0.3% Top 5 Holders 2,679,674 22.3% *Calculated on the basis of 11,997,447 common shares outstanding on M arch 27, 2018 Source: Company reports and Bloomberg

6% Convertible Exchangeable Preferred Stock

As of June 30, 2018, CYCC had 335,273 shares of 6% convertible exchangeable preferred stock. Prior to conversion the preferred stock has no maturity date and no voting rights. CYCC may redeem the preferred stock at the redemption price of $10.00 per share.

Recent Equity Issuances

July 2017: CYCC raised $13.7M through the issuance of common stock, preferred stock and warrants. Each unit was priced at $2 and included a 7-year warrant with an exercise price of $2.00. The class A units included 1 share of common stock while class B units contained convertible preferred stock of comparable economic value. On net, the transaction resulted in the issuance of 7.5 million shares and an equivalent number of warrants. Over the past three years the company has also raised $5.3M through issuance of common stock through an ATM facility.

1:12 Reverse Stock Split

In May 2016, CYCC completed a one-for-twelve reverse stock split.

TAXES

CYCC has operating activities in both the United States and the United Kingdom. As such, the company incurs operating expenses and related tax assets in both jurisdictions. Based on the company’s current corporate structure, in our view, management retains significant flexibility on whether future operating profits flow through the U.S. or U.K. operations. To

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the extent CYCC chooses to partner CYC065 or other pipeline programs, in our view, agreements allowing royalty income to flow through the U.K. operations may offer better near-term tax efficiencies due to higher tax asset balances and operating expenses in the U.K.

As of December 31, 2017, CYCC had U.S. federal net operating loss carryforwards of $28.4M that will begin expiring in 2026. We believe tax assets accrued prior to the July 2017 financing may be subject to 382 impairment under U.S. tax code and not available to offset future losses.

The company’s foreign subsidiary in the United Kingdom has tax loss carryforwards of $186.2M. CYCC’s foreign NOLs do not expire under U.K. tax law. However, for losses created after April 1, 2017, the use of these NOLs may be restricted with a cap of 50% of profits in any one year.

In total, we expect the company to accrue an additional $60M-$100M of additional NOLs prior to reaching profitability with most of the losses reported in the U.K.

Based on our financial projections, we expect current and future tax assets to offset the first 2 years of profitability (through 2024). For subsequent periods we expect the company to recognize an effective tax rate of 30%.

FINANCIAL MODELING ASSUMPTIONS

CYCC is a development-stage company and is unlikely to generate material product revenues until launch of CYC065 in 2023. As such, we do not view CYCC as an EPS- driven story and encourage investors to focus on clinical and business development as the primary avenues for near-to-intermediate term shareholder value creation.

We expect the cash burn rate to increase over the next several quarters as the company accelerates clinical development of CYC065 in combination with venetoclax for treatment of relapsed/refractory CLL and potentially moves the PLK1 inhibitor CYC140 into Phase I development. By our estimates, CYCC should burn $9M in 2018 and $11M in 2019. CYCC ended June 2018 with $19.8M in cash, which, in our view, should fund operations into 1H20.

Sales. We do not expect the company to begin receiving material revenues until potential commercial launch of CYC065 in 2023. Our model assumes the company recognizes all revenues in the U.S. and collects royalty revenue in other geographies.

COGS. We expect CYC065 to enjoy typical gross margins for an oral oncology therapy of 90%+ once sales reach critical mass.

G&A. We expect G&A expenses to increase in 2018 to $5.4M from $5.3M in 2017 as growth in salaries is partially offset by the absence of one-time expenses associated with recapitalization of the balance sheet in 2Q17. Moving forward, we expect administrative expenses to increase at an annual rate of 10%-12%.

Sales and Marketing. We do not expect CYCC to incur meaningful sales and marketing expense until 2023. Our model calls for the company to hire 25 sales people to support the U.S. launch of CYC065 and build a field sales force of about 40 reps within 2 years of launch. In total, we expect peak sales and marketing expense of $18M-$22M annually.

R&D. Our forecast calls for a modest acceleration in R&D spending over the next several quarters driven by clinical advancement of CYC065 partially offset by continued reduction of spending for sapacitabine. We forecast spending of $3.9M in 2018 and $5.0M in 2019.

EPS. We expect CYCC to record earnings per share of ($0.71) for 2018 and ($0.91) for 2019. We expect the company to achieve profitability in 2023 or 2024.

Share Count. Following a 1:12 reverse stock split in May 2016 and recapitalization of the balance sheet in July 2017, we estimate CYCC has 12.0 million shares outstanding.

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MANAGEMENT

As of March 27, 2018, CYCC used a semi-virtual development model with 12 full-time employees and a network of partners to support certain manufacturing and clinical trials activities. Most of the senior leadership has been with CYCC for over a decade and, in our view, the management structure is appropriate for near-term development of CYC065. Over the next 2-3 years we expect the company to make modest additions to the clinical/regulatory team.

Chief Executive Officer: Spiro Rombotis has guided CYCC through much of its corporate evolution since joining the company in 1997. He currently serves as President and CEO. Prior to CYCC, most of his experience was with large pharmaceutical companies including as Vice President, International Operations and Business Development at The Liposome Company, which was subsequently acquired by Elan in 2000 for $575M. Earlier in his career Mr. Rombotis worked at Bristol-Myers Squibb Co. as Vice President, Pharmaceuticals Central and Eastern Europe, the Centocor group of Johnson & Johnson as Head of European Marketing and Sales, and in business development for Novartis. He holds a BA from Williams College and an MBA in Hospital Management from the Kellogg Graduate School of Management. He also serves on the Board of Trustees of BioNJ.

Finance: Paul McBarron joined CYCC in January 2002 after previously working in a senior finance role at Shire Pharmaceuticals for 5 years. He currently serves as Chief Operating Officer, Chief Financial Officer, Executive Vice President of Finance and Secretary at the company. Earlier in his career, Mr. McBarron worked in finance positions at Sterling Drug, Sanofi-Winthrop, now part of Sanofi and SmithKline Beecham, now part of GlaxoSmithKline. He is a chartered accountant and previously worked at Ernst & Young. Mr. McBarron served on the Life Sciences Industry Advisory Board for the Scottish Government.

Chief Scientist: David Glover joined CYCC in November 1999 and continues to split his interests between academic topics and corporate biotechnology. In addition to his responsibilities at the company, he is the Arthur Balfour Professor of Genetics and Chairman in the Department of Genetics at the University of Cambridge and Director of Cancer Research at UK Cell Cycle Genetics Research Group. Dr. Glover was previously Professor of Molecular Genetics at the University of Dundee and Professor and Head of Biochemistry at Imperial College, London. He is a member of the European Molecular Biology Organization and has authored over 200 publications.

Clinical Development and Regulatory Affairs: In 2004 Judy Chiao joined CYCC as Vice President, Clinical Development and Regulatory Affairs. She has prior experience in both clinical development and regulatory affairs including as a leader of clinical development for the HDAC inhibitor Zolinza for Aton Pharma, which was acquired by Merck & Co in 2004. Dr. Chiao also worked at FDA as a Senior Medical Reviewer for ODAC. She earned her BS in Chemistry from Columbia University and MD from Harvard Medical School.

PRIMARY RISKS We think the primary risks of an investment in CYCC shares include, but are not limited to:

Clinical Trial: While CYCC has significant experience designing and conducting large scale pivotal clinical trials, there can be no assurance future combination studies of CYC065 will be sufficient to support continued development. If CYCC cannot design efficient clinical trials, development of CYC065 and other pipeline programs may not meet expected timelines. Additionally, there can be no assurance any future studies of pipeline programs will replicate prior results or be adequate to support regulatory approval, reimbursement, partnerships, or general commercial acceptance by clinicians. Furthermore, CYCC or a future partner may need to conduct post-marketing studies to support full regulatory approval. Lastly, CYCC relies on a virtual clinical development business model based on a small in-house management team and third party contractors. Loss of one or more executives could have an adverse impact on management of future clinical trials.

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Manufacturing: CYCC uses third-party CMOs to manage its supply chain for CYC065 and other pipeline programs. There can be no assurance existing or future third-party CMO relationships will provide adequate commercial production of CYC065 to support clinical trials and future commercial demand. Disruption in third-party manufacturing supply chain, including single source production of API and pharmaceutical product, could adversely impact sales and the company’s balance sheet.

Regulatory: CYCC is subject to oversight by regulators in several jurisdictions including Japan’s Pharmaceuticals and Medical Devices Agency and U.S. FDA and EMA in Europe. There can be no assurance ongoing clinical studies will be adequate to support a future NDA filing for CYC065 or sapacitabine. Additionally, failure to maintain regulatory clearance for approved products could adversely impact the company’s revenues. Finally, sapacitabine failed to meet the primary endpoint of overall survival in Phase III development for AML. There can be no assurance regulators will accept alternative endpoints to support regulatory filing of sapacitabine.

Competition: While many companies are developing CDK 4/6 inhibitors for treatment of breast cancer and other solid tumors, CYC065 is one of the few drug candidates in development against CDK 9. There can be no assurance the clinical profile of CYC065 will be sufficiently differentiated from other CDK inhibitors to enjoy commercial adoption, particularly in solid tumors. Furthermore, several pharmaceutical and biotechnology companies have nucleoside analogs or other products on the market or in clinical trials which may be competitive to sapacitabine in both hematology and solid tumor indications. There can be no assurance CYCC will effectively develop CYC065 and sapacitabine against these existing and future competitors.

Intellectual Property: CYCC has 25 U.S. patents, 14 patents granted by the European Patent Office and 59 granted patents in other countries. Additionally, the company has licensed 48 granted patents, one patent application pending in the United States, and 18 patent applications pending in other countries. Sapacitabine is protected by composition of matter patents for the U.S. into 2022, excluding patent extensions. CYC065 enjoys composition of matter protection through 2031 in the U.S. There can be no assurance CYCC will be able to maintain or extend patent protection or that changes to patent law or interpretation will not adversely impact the company’s future revenues.

CROs and Third-Party Clinical Trial Support: CYCC has historically relied on partnerships with research institutions and contract service providers to support development of its pipeline programs. There can be no assurance current partners will be successful in maintaining a steady supply of drug product, provide adequate support for preclinical development or provide adequate support for clinical trial enrollment.

Product Liability: Biotech companies may face potential product liability lawsuits associated with adverse events – both currently identified and identified through future clinical trials and commercial experience. The company’s commercial manufacturing facilities are subject to significant environmental, health and safety regulation. Additionally, any future commercial practices in the U.S. will be subject to Department of Justice regulations prohibiting promotion of vaccines or therapeutics for indications beyond the intended use described in the package insert. Product liability claims may result in limiting future product promotion, removal of one or more products from the market and potential for financial penalties and fines that may adversely impact CYCC’s cash flow and financial position, including cash balance.

Currency: The functional and reporting currency for CYCC is the United States dollar. However, some of the company’s operating expenses are denominated in foreign currencies, including the British Pound for research and development costs associated with CYCC’s United Kingdom-based subsidiary. Consequently, changes in exchange rates, particularly weakening of the United States dollar relative to British pound, may adversely affect operating expenses and cash burn for the company.

Shareholder Concentration: Three institutional investors control more than 24% of the company's outstanding capital stock, including an 18% stake for Eastern Capital. This shareholder concentration may have significant influence over the outcome of corporate

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actions including future discussions regarding financing, commercial operations and potential change of control.

Healthcare Reform: Healthcare reform and its restrictions on coverage and reimbursement may adversely affect CYCC’s business.

International Expansion: CYCC is exposed to risks associated with doing business outside of the U.S. including laws and regulations that may preclude development, manufacture, and sale of CYCC’s product candidates outside U.S. or require costly compliance programs.

Potential for Ongoing Losses: We expect CYCC to incur significant operating losses until the potential launch of CYC065. These expected operating losses are likely to exceed the company’s current access to capital. There can be no assurance sales of CYC065 will be adequate to support our financial outlook for the company to achieve profitability in 2023 or 2024.

Currency: The functional and reporting currency for CYCC is the United Stated dollar. However, some of the company’s operating expenses associated with R&D are denominated in foreign currency including the British Pound. While the exchange rate of the British pound to U.S. dollar has historically been relatively stable, there can be no assurance future volatility in currency exchange rates will not materially impact the cost of funding the company’s operations.

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Table 17. CYCC Income Statement

Cyclacel Pharmaceuticals Income Statement (in $ millions) 2017A 1Q18A 2Q18A 3Q18E 4Q18E 2018E 2019E CYC065 $0.0 $0.0 $0.0 $0.0 $0.0 $0.0 $0.0 Partner revenue 0.0 0.0 0.0 0.0 0.0 0.0 0.0 Total product revenue 0.0 0.0 0.0 0.0 0.0 0.0 0.0 Other Revenue 0.0 0.0 0.0 0.0 0.0 0.0 0.0 Total Revenue $0.0 $0.0 $0.0 $0.0 $0.0 $0.0 $0.0

COGS 0.0 0.0 0.0 0.0 0.0 0.0 0.0

Gross profit $0.0 $0.0 $0.0 $0.0 $0.0 $0.0 $0.0

G&A 5.3 1.4 1.3 1.2 1.6 5.4 5.9 Research & development 4.2 0.8 1.2 1.0 1.0 3.9 5.0 Operating profit (loss) ($9.5) ($2.2) ($2.5) ($2.2) ($2.5) ($9.3) ($10.9)

Interest expense 0.0 0.0 0.0 0.0 0.0 0.0 0.0 Other 0.9 0.6 0.0 0.0 0.0 0.6 0.0

Net profit (loss) (8.4) (1.5) (2.4) (2.2) (2.5) (8.5) (10.9)

Earnings (loss) per share from continuing ops ($1.10) ($0.13) ($0.20) ($0.18) ($0.21) ($0.71) ($0.91)

One-time items (6.221) 0.182 0.502 0.000 0.000 0.684 0.000 Dividend on convertible exchangeable preferred shares (0.201) (0.050) (0.050) 0.000 0.000 (0.100) 0.000

Net income (loss) as reported (14.8) (1.4) (1.9) (2.2) (2.5) (8.0) (10.9)

Earnings (loss) per share as reported ($1.95) ($0.12) ($0.16) ($0.18) ($0.21) ($0.66) ($0.91)

Weighted average common shares 7.6 12.0 12.0 12.0 12.0 12.0 12.0 Source: Company reports and Ladenburg Thalmann estimates

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Table 18. CYCC Balance Sheet

Cyclacel Pharmaceuticals Balance Sheet (in $ millions) 1Q17A 2Q17A 3Q17A 4Q17A 1Q18A 2Q18A Assets Cash and short term investment $12.7 $13.6 $26.0 $23.9 $21.7 $19.8 Other 4.3 2.5 1.8 2.1 3.0 2.9 Total current assets $17.0 $16.1 $27.8 $26.0 $24.7 $22.7

Total assets $17.1 $16.1 $27.9 $26.0 $24.8 $22.7

Liabilities Accounts payable $1.7 $2.0 $2.0 $1.6 $1.9 $1.7 Other accrued liabilities 2.5 2.3 2.3 2.6 2.3 2.3 Total current liabilities $4.1 $4.3 $4.3 $4.1 $4.3 $4.0

Other $0.1 $0.1 $0.1 $0.1 $0.1 $0.1 Total liabilities $4.3 $4.4 $4.4 $4.2 $4.4 $4.1

Shareholder equity Paid-in capital $350.2 $351.2 $364.9 $365.1 $365.1 $365.1 Accumulated other comprehensive income (0.7) (0.7) (0.8) (0.8) (0.8) (0.8) Accumulated deficit (336.6) (338.8) (340.6) (342.5) (343.9) (345.7) Total shareholder equity $12.8 $11.6 $23.5 $21.8 $20.4 $18.6 Source: Company Reports

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APPENDIX A: IMPORTANT RESEARCH DISCLOSURES

ANALYST CERTIFICATION I, Kevin DeGeeter, attest that the views expressed in this research report accurately reflect my personal views about the subject security and issuer. Furthermore, no part of my compensation was, is, or will be directly or indirectly related to the specific recommendation or views expressed in this research report, provided, however, that: The research analyst primarily responsible for the preparation of this research report has or will receive compensation based upon various factors, including the volume of trading at the firm in the subject security, as well as the firm’s total revenues, a portion of which is generated by investment banking activities. Additional information regarding the contents of this publication will be furnished upon request. Please contact Ladenburg Thalmann, Compliance Department, 277 Park Avenue, 26th floor, New York, New York 10172 (or call 212-409-2000) for any information regarding current disclosures, and where applicable, relevant price charts, in regard to companies that are the subject of this research report.

COMPANY BACKGROUND Cyclacel is a clinical stage biotechnology company developing oncology drugs based on cell cycle regulation, transcriptional regulation and DNA damage response. The company’s research activity is focused on CYC065, a CDK2/9 inhibitor in Phase I development for relapsed/ refractory CLL. The company's early-stage pipeline includes CYC140, a PLK1 inhibitor. The Berkeley Heights, NJ-based company retains global rights to each of its drug candidates.

VALUATION METHODOLOGY Our $6.25 price target is based on a DCF analysis assuming a 32% discount rate, 20.3 million shares on a fully diluted basis, terminal year (2025) FCF of $177M and 13% long term revenue growth rate.

RISKS These risk factors (intellectual property, regulatory, reimbursement, partnership, and financing) do not constitute all the potential risks of investing in the subject company’s shares. Investors should refer to the company’s SEC filings including the most recent forms 10-K and 10- Q for further details on the risks associated with an investment in the subject company’s shares.

STOCK RATING DEFINITIONS Buy: The stock’s return is expected to exceed 12.5% over the next twelve months. Neutral: The stock’s return is expected to be plus or minus 12.5% over the next twelve months. Sell: The stock’s return is expected to be negative 12.5% or more over the next twelve months. Investment Ratings are determined by the ranges described above at the time of initiation of coverage, a change in risk, or a change in target price. At other times, the expected returns may fall outside of these ranges because of price movement and/or volatility. Such interim deviations from specified ranges will be permitted but will become subject to review.

RATINGS DISPERSION AND BANKING RELATIONSHIPS AS OF (September 7, 2018)

Rating % IB % BUY 80.1 53.3 NEUTRAL 19.9 43.9 SELL 0.0 0.0

COMPANIES UNDER KEVIN'S COVERAGE ADMA Biologics, Inc. (ADMA) Aviragen Therapeutics, Inc. (AVIR) BioTime, Inc. (BTX) Catalyst Biosciences, Inc. (CBIO) Cidara Therapeutics, Inc. (CDTX) ContraFect Corporation (CFRX) Curetis N.V. (CURE.NA) Cyclacel Pharmaceuticals, Inc. (CYCC) Exact Sciences Corporation (EXAS) Genomic Health Inc. (GHDX) Interpace Diagnostics Group, Inc. (IDXG) Kindred Biosciences, Inc. (KIN) Mesoblast Ltd. (MESO) Melinta Therapeutics Inc. (MLNT) Molecular Templates, Inc. (MTEM) Novavax, Inc. (NVAX) Invitae Corporation (NVTA) Opko Health, Inc. (OPK) Paratek Pharmaceuticals, Inc. (PRTK) Synergy Pharmaceuticals Inc. (SGYP) VBI Vaccines, Inc. (VBIV) Vericel Corporation (VCEL)

Page 29 Kevin DeGeeter 212.409.2027 Cyclacel Pharmaceuticals, Inc. (CYCC)

COMPANY SPECIFIC DISCLOSURES Ladenburg Thalmann & Co. Inc. makes a market in Cyclacel Pharmaceuticals, Inc..

INVESTMENT RATING AND PRICE TARGET HISTORY Cyclacel Pharmaceuticals, Inc. Rating History as of 09/06/2018 powered by: BlueMatrix

14 12 10 8 6 4 2 0 Oct 2015 Jan 2016 Apr 2016 Jul 2016 Oct 2016 Jan 2017 Apr 2017 Jul 2017 Oct 2017 Jan 2018 Apr 2018 Jul 2018

B=Buy N=Neutral S=Sell D=Drop Coverage I=Initiate NR=Not Rated

GENERAL DISCLAIMERS Information and opinions presented in this report have been obtained or derived from sources believed by Ladenburg Thalmann & Co. Inc. to be reliable. The opinions, estimates and projections contained in this report are those of Ladenburg Thalmann as of the date of this report and are subject to change without notice. Ladenburg Thalmann & Co. Inc. accepts no liability for loss arising from the use of the material presented in this report, except that this exclusion of liability does not apply to the extent that such liability arises under specific statutes or regulations applicable to Ladenburg Thalmann & Co. Inc. This report is not to be relied upon in substitution for the exercise of independent judgment. Ladenburg Thalmann & Co. Inc. may have issued, and may in the future issue, other reports that are inconsistent with, and reach different conclusions from, the information presented in this report. Those reports reflect the different assumptions, views and analytical methods of the analysts who prepared them and Ladenburg Thalmann & Co. Inc. is under no obligation to ensure that such other reports are brought to the attention of any recipient of this report. Investors should consider this report as only a single factor in making their investment decisions. Some companies that Ladenburg Thalmann & Co. Inc. follows are emerging growth companies whose securities typically involve a higher degree of risk and more volatility than the securities of more established companies. The securities discussed in Ladenburg Thalmann & Co. Inc. research reports may not be suitable for some investors. Investors must make their own determination as to the appropriateness of an investment in any securities referred to herein, based on their specific investment objectives, financial status and risk tolerance. Past performance should not be taken as an indication or guarantee of future performance, and no representation or warranty, express or implied, is made regarding future performance. The price, value of and income from any of the securities mentioned in this report can fall as well as rise. The value of securities is subject to exchange rate fluctuation that may have a positive or adverse effect on the price or income of such securities. Investors in securities such as ADRs, the values of which are influenced by currency volatility, effectively assume this risk. Securities recommended, offered or sold by Ladenburg Thalmann & Co. Inc. (1) are not insured by the Federal Deposit Insurance Company; (2) are not deposits or other obligations of any insured depository institution; and (3) are subject to investment risks, including the possible loss of some or all of principal invested. Indeed, in the case of some investments, the potential losses may exceed the amount of initial investment and, in such circumstances; you may be required to pay more money to support these losses. The information and material presented in this report are provided to you for information purposes only and are not to be used or considered as an offer or the solicitation of an offer to sell or to buy any securities mentioned herein. This publication is confidential for the information of the addressee only and may not be reproduced in whole or in part, copies circulated, or disclosed to another party, without the prior written consent of Ladenburg Thalmann & Co. Inc.

Investing in low priced securities is speculative and carries a high degree of risk. You should independently investigate and understand all risks before making any investment. The markets for small cap stocks are highly speculative and this level of risk may not be appropriate for all investors. Some of the companies listed may be subject to the “Penny Stock Rule”. Under this rule, the SEC has defined a “penny stock” to be an equity security which has a market price of less than $5.00 a share, subject to certain exemptions. Such exemptions include equity listed on NASDAQ and an equity security issued by an issuers which has (i) net tangible assets of at least $2,000,000, if such issuers has

Page 30 Kevin DeGeeter 212.409.2027 Cyclacel Pharmaceuticals, Inc. (CYCC) been in continuous operational for (3) years; (ii) net tangible assets of $5,000,000, if such issuer has been in continuous operation for less than (3) years; or (iii) average revenue of at least $6,000,000 for the preceding three (3) years. Unless such exemption is available, regulations require delivery of a risk disclosure document explaining the penny stock market and the risks associated therewith prior to any transaction involving a penny stock. For stock not quoted on NASDAQ or at any time that the company has less than $2,000,000 in net tangible assets, the trading in common stock is covered under Rule 15g-9 under the Securities Exchange Act of 1934 for non-NASDAQ and non-exchange listed securities. Under such rule, broker-dealers who recommend covered securities to persons other than established customers and accredited investors must make a written suitability determination for the purchaser and receive the purchaser’s written agreement to a transaction prior to sale. Some securities may not be cleared for sale in all states or other jurisdictions and LTCO assumes no responsibility to apprise you of individual states and jurisdictions’ regulatory restrictions. Stocks in the microcap segment of market have risks that are not as common in other segments of market. These risks include, but are not limited to, liquidity risk, which can lead to higher volatility and low trade volume, company specific risks that contribute to lower valuation, higher probability of financial default and distress.

Member: NYSE, NYSE American, NYSE Arca, FINRA, all other principal exchanges and SIPC Additional Information Available Upon Request ©2018 - Ladenburg Thalmann & Co. Inc. All Rights Reserved.

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EQUITY RESEARCH

ENERGY, POWER & INFRASTRUCTURE

Energy Exploration & Production, Upstream Michael Schmitz, CFA (212) 409-2028 [email protected] Master Limited Partnerships, Midstream Michael Schmitz, CFA (212) 409-2028 [email protected]

HEALTHCARE

Biotechnology Matthew L. Kaplan (212) 891-5247 [email protected]

Biotechnology Wangzhi Li, PhD (212) 409-2051 [email protected] Biotechnology (Personalized Medicine) Kevin DeGeeter (212) 409-2027 [email protected]

Biopharmaceuticals Michael Higgins (212) 409-2074 [email protected] Rui Galvao, PhD (212) 409-2075 [email protected]

Healthcare Equipment & Medical Technologies Jeffrey S. Cohen (561) 620-2049 [email protected]

FINANCIAL INSTITUTIONS

Financial Services – Business Development Co. & Specialty Finance Mickey M. Schleien, CFA (305) 572-4131 [email protected] Financial Services – Business Development Co. & Specialty Finance Christopher Nolan, CFA (212) 409-2068 [email protected] Financial Services – Equity REITs John J. Massocca (212) 409-2543 [email protected]

TECHNOLOGY

Internet & Software Services Jon R. Hickman (510) 918-4045 [email protected] Software and Services Glenn G. Mattson (212) 409-2073 [email protected]

ADDITIONAL CONTACTS Kenneth Brush, Head of Trading (212) 409-2011 [email protected] Eric Novotny (212) 409-2011 [email protected]

277 Park Avenue 26th Floor New York, NY 10172 (212) 409-2000