Treatment of Melanoma and Breast Cancer

Total Page：16

File Type：pdf, Size：1020Kb

Request title: Treatment of melanoma and breast cancer Reference Number: F2739 Date of Response: 23/11/2020 Further to your Freedom of Information Act request, please find the Trust’s response, in blue bold text below: Request and Royal Devon and Exeter NHS Foundation Trust Response 1. How many patients are currently (past 3 months) undergoing treatment for melanoma, and how many of these are BRAF+ ? 108. Please note this will include same patients receiving primary and then any subsequent treatment in the period range) *≤5 patients recorded as BRAF+ *Five ≤5. In accordance with section 40 (2) of the Freedom of Information Act 2000, we are unable to provide figures where the number of patients is less than or equal to five and could risk the identification of those patients and breach Caldicott principles. This follows NHS Digital (formerly HSCIC) analysis guidance (2014) which states that small numbers within local authorities, wards, postcode districts, CCG’s providers and Trusts may allow identification of patients and should not be published. 2. For patients currently (past 3 months) under treatment for melanoma How many patients are Stage IIIa? *Five ≤5. How many patients are Stage III resectable?. All of the patients How many Stage III patients received a complete resection in the past 3 months? All of the above patients. 3. In the past 3 months, how many melanoma patients were treated with the following: · Bevacizumab – 0 patients · Cobimetinib – 0 patients · Dabrafenib – ≤5 patients · Dabrafenib AND Trametinib – 11 patients · Dacarbazine – 0 patients · Encorafenib AND Binimetinib – 0 patients · Ipilimumab – 0 patients · Ipilimumab AND Nivolumab – ≤5patients · Nivolumab – 35 patients · Pembrolizumab – 15 patients · Trametinib – 0 patients · Vemurafenib – 0 patients · Vemurafenib AND Cobimetinib – 0 patients · Other active systemic anti-cancer therapy – ≤5 patients on other chemo care · Palliative care only · Palliative care only *Five ≤5 Specialist Palliative Care 4. In the past 3 months how many patients were treated with the following for breast cancer? · Abemaciclib + Anastrozole/Exemestane/Letrozole – 0 patients · Abemaciclib + Fulvestrant – 13 patients · Alpelisib + Fulvestrant – 0 patients · Atezolizumab – ≤5 patients · Bevacizumab – 0 patients · Eribulin – ≤5 patients · Everolimus + Exemestane – ≤5 patients · Fulvestrant as a single agent – 0 patients · Gemcitabine + Paclitaxel – 0 patients · Lapatinib – ≤5 patients · Neratinib – ≤5 patients · Olaparib – ≤5 patients · Palbociclib + Anastrozole/Exemestane/Letrozole – 24 patients · Palbociclib + Fulvestrant – ≤5 patients · Pertuzumab + Trastuzumab + Docetaxel – ≤5 patients · Ribociclib + Anastrozole/Exemestane/Letrozole – 11 patients · Ribociclib + Fulvestrant – 8 patients · Talazoparib – 0 patients · Transtuzumab + Paclitaxel – ≤5 patients · Transtuzumab as a single agent – 24 patients (trastuzumab) · Trastuzumab emtansine – 7 patients · Any other active systemic anti-cancer therapy – 123 patients on other chemo care .

Copy Link

Recommended publications

Oncofocus® Precision Oncology
Medical Laboratory Accredited to ISO15189:2012 Oncofocus® Precision Oncology ONCOFOCUS® TEST REPORT Oncologica UK Ltd Suite 15-16, The Science Village Chesterford Research Park Cambridge, CB10 1XL, UK Tel: +44(0)1223 785327 Email: [email protected] Lead Clinical Scientist: - Pre-Reg Clinical Scientist: - Date: 1 of 30 ONC19 - Surname - Requester - Forename - Contact details - DOB - Date requested - Gender - Histology # - Tumour % - Primary site Breast Tumour % - Tumour subtype - (macrodissected) Tissue Type - Comment: The DNA and RNA extracted from this sample were of optimal quality. The Oncofocus assay on which the sample was run met all assay specific quality metrics. Oncofocus currently targets 505 genes covering oncogenes, fusion genes, genes susceptible to copy number variation and tumour suppressors. Actionable genetic variants detected by Oncofocus are currently linked to 687 anti-cancer targeted therapies/therapy combinations. The following actionable variants were detected: Within the 'Current Clinical Trials Information' section of this report, starting on page 8, the NCT numbers are hyperlinks to the clinicaltrials.gov webpages which should be accessed to gain further trial specific information Sample Cancer Type: Breast Cancer Clinically Significant Biomarkers Indicated Contraindicated Relevant Therapies Relevant Therapies Genomic Alteration Alt allele freq (In this cancer type) (In other cancer type) Clinical Trials ERBB2 p.(G727A) c.2180G>C 39% Clinical trials and/or off-label ado-trastuzumab emtansine 19 BRAF p.(V600E) c.1799T>A 5% Clinical trials and/or off-label dabrafenib 13 vemurafenib PIK3CA p.(G1049R) c.3145G>C 58% Clinical trials and/or off-label Clinical trials and/or off-label 15 Sources included in relevant therapies: EMA1, FDA2, ESMO, NCCN Hotspot variants with >10% alternate allele reads are classified as ‘detected’ with an assay sensitivity and positive predictive value(PPV) of 99%.
[Show full text]
Identification of Recurrent Mutational Events in Anorectal Melanoma
Modern Pathology (2017) 30, 286–296 286 © 2017 USCAP, Inc All rights reserved 0893-3952/17 $32.00 Identification of recurrent mutational events in anorectal melanoma Hui Min Yang1,2,6, Susan J Hsiao1,6, David F Schaeffer2, Chi Lai3, Helen E Remotti1, David Horst4, Mahesh M Mansukhani1 and Basil A Horst1,5 1Department of Pathology & Cell Biology, Columbia University Medical Center, New York, NY, USA; 2Department of Pathology & Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada; 3Department of Pathology and Laboratory Medicine, University of Ottawa, Ottawa, ON, Canada; 4Pathologisches Institut, Ludwig-Maximilians-Universitaet, Muenchen, Germany and 5Department of Dermatology, Columbia University Medical Center, New York, NY, USA Anorectal melanoma is a rare disease that carries a poor prognosis. To date, limited genetic analyses confirmed KIT mutations as a recurrent genetic event similar to other mucosal melanomas, occurring in up to 30% of anorectal melanomas. Importantly, a subset of tumors harboring activating KIT mutations have been found to respond to c-Kit inhibitor-based therapy, with improved patient survival at advanced tumor stages. We performed comprehensive targeted exon sequencing analysis of 467 cancer-related genes in a larger series of 15 anorectal melanomas, focusing on potentially actionable variants based on gain- and loss-of-function mutations. We report the identification of oncogenic driver events in the majority (93%) of anorectal melanomas. These included variants in canonical MAPK pathway effectors rarely observed in cutaneous melanomas (including an HRAS mutation, as well as a BRAF mutation resulting in duplication of threonine 599), and recurrent mutations in the tumor suppressor NF1 in 20% of cases, which represented the second-most frequently mutated gene after KIT in our series.
[Show full text]
Product Monograph Including Patient Medication Information
PRODUCT MONOGRAPH INCLUDING PATIENT MEDICATION INFORMATION Pr ® COTELLIC cobimetinib tablets 20 mg cobimetinib (as cobimetinib fumarate) Protein Kinase Inhibitor Date of Revision: Hoffmann-La Roche Limited January 5, 2018 7070 Mississauga Road Mississauga, Ontario, Canada L5N 5M8 www.rochecanada.com Submission Control No: 209926 COTELLIC®, ZELBORAF® are registered trade-marks of F. Hoffmann-La Roche AG, used under license ©Copyright 2016-2017, Hoffmann-La Roche Limited Page 1 of 38 Table of Contents PART I: HEALTH PROFESSIONAL INFORMATION .........................................................3 SUMMARY PRODUCT INFORMATION ........................................................................3 INDICATIONS AND CLINICAL USE ..............................................................................3 CONTRAINDICATIONS ...................................................................................................3 WARNINGS AND PRECAUTIONS ..................................................................................4 ADVERSE REACTIONS ..................................................................................................11 DRUG INTERACTIONS ..................................................................................................15 DOSAGE AND ADMINISTRATION ..............................................................................17 OVERDOSAGE ................................................................................................................20 ACTION AND CLINICAL PHARMACOLOGY ............................................................20
[Show full text]
Quantification of Cobimetinib, Cabozantinib, Dabrafenib, Niraparib
University of Groningen Quantification of cobimetinib, cabozantinib, dabrafenib, niraparib, olaparib, vemurafenib, regorafenib and its metabolite regorafenib M2 in human plasma by UPLC-MS/MS Krens, Stefanie D; van der Meulen, Eric; Jansman, Frank G A; Burger, David M; van Erp, Nielka P Published in: Biomedical chromatography DOI: 10.1002/bmc.4758 IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite from it. Please check the document version below. Document Version Publisher's PDF, also known as Version of record Publication date: 2020 Link to publication in University of Groningen/UMCG research database Citation for published version (APA): Krens, S. D., van der Meulen, E., Jansman, F. G. A., Burger, D. M., & van Erp, N. P. (2020). Quantification of cobimetinib, cabozantinib, dabrafenib, niraparib, olaparib, vemurafenib, regorafenib and its metabolite regorafenib M2 in human plasma by UPLC-MS/MS. Biomedical chromatography, 34(3), [4758]. https://doi.org/10.1002/bmc.4758 Copyright Other than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons). The publication may also be distributed here under the terms of Article 25fa of the Dutch Copyright Act, indicated by the “Taverne” license. More information can be found on the University of Groningen website: https://www.rug.nl/library/open-access/self-archiving-pure/taverne- amendment. Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim.
[Show full text]
RP - HPLC Method Development & Validation for the Simultaneous Estimation of Encorafenib and Binimetinib in API & Tablet Dosage Form
International Journal of Science and Research (IJSR) ISSN: 2319-7064 ResearchGate Impact Factor (2018): 0.28 | SJIF (2018): 7.426 RP - HPLC Method Development & Validation for the Simultaneous Estimation of Encorafenib and Binimetinib in API & Tablet Dosage Form Kafiya Suroor1, Kudaravalli Sreedevi2 Department of Quality Assurance, Sultan –ul-Uloom College of Pharmacy, Hyderabad, India Abstract: A new RP-HPLC method was developed, validated and adapted for the estimation of encorafenib and binimetinib in bulk and tablet formulation. In this method, separation and assay of encorafenib and binimetinib was done in stationary phase using Agilent C18 column with mobile phase of 0.1M dipotassium hydrogen phosphate (pH 4.0) and methanol in 50:50 vol/vol ratio. The Binimetinib was eluted at 3.448 min and encorafenib at 5.795 min. Linearity ranges are 7.5-22.5 μg/ml and 37.5-112.50 μg/ml with regression coefficient values of 0.9996 and 0.9997 for binimetinib and encorafenib respectively. The LOD values found were binimetinib – 0.017 µg/ml and encorafenib – 0.114 µg/ml, and the LOQ values of binimetinib – 0.058 µg/ml and encorafenib – 0.381 µg/ml. Validation parameters examined following suggestions of ICH are accurate ample for the supposed assay. The approach is confirmed as splendid method for assay of encorafenib and binimetinib in tablet formula with excellent assay percentage values. Keywords: RP-HPLC, Encorafenib, Binimetinib, Antineoplastic drugs 1. Introduction dose of binimetinib is 45 mg orally twice daily and of encorafenib is 450 mg orally once daily. Approval by FDA Encorafenib and Binimetanib belong to the class of was based on a randomized, active-controlled, open-label, antineoplastic agents.
[Show full text]
Mekinist, INN-Trametinib
ANNEX I SUMMARY OF PRODUCT CHARACTERISTICS 1 This medicinal product is subject to additional monitoring. This will allow quick identification of new safety information. Healthcare professionals are asked to report any suspected adverse reactions. See section 4.8 for how to report adverse reactions. 1. NAME OF THE MEDICINAL PRODUCT Mekinist 0.5 mg film-coated tablets Mekinist 2 mg film-coated tablets 2. QUALITATIVE AND QUANTITATIVE COMPOSITION Mekinist 0.5 mg film-coated tablets Each film-coated tablet contains trametinib dimethyl sulfoxide equivalent to 0.5 mg of trametinib. Mekinist 2 mg film-coated tablets Each film-coated tablet contains trametinib dimethyl sulfoxide equivalent to 2 mg of trametinib. For the full list of excipients, see section 6.1. 3. PHARMACEUTICAL FORM Film-coated tablet Mekinist 0.5 mg film-coated tablets Yellow, modified oval, biconvex, film-coated tablets, approximately 4.8 x 8.9 mm, with “GS” debossed on one face and “TFC” on the opposing face. Mekinist 2 mg film-coated tablets Pink, round, biconvex, film-coated tablets, approximately 7.5 mm, with “GS” debossed on one face and “HMJ” on the opposing face. 4. CLINICAL PARTICULARS 4.1 Therapeutic indications Trametinib as monotherapy or in combination with dabrafenib is indicated for the treatment of adult patients with unresectable or metastatic melanoma with a BRAF V600 mutation (see sections 4.4 and 5.1). Trametinib monotherapy has not demonstrated clinical activity in patients who have progressed on a prior BRAF inhibitor therapy (see section 5.1). 4.2 Posology and method of administration Treatment with trametinib should only be initiated and supervised by a physician experienced in the administration of anti-cancer medicinal products.
[Show full text]
Successful Chemotherapy Is Possible for Seemingly Inoperable Anaplastic Thyroid Cancer
® Clinical Thyroidology for the Public VOLUME 12 | ISSUE 12 | DECEMBER 2019 THYROID CANCER Successful chemotherapy is possible for seemingly inoperable anaplastic thyroid cancer BACKGROUND form of standard chemotherapy and 2 received another While the vast majority of thyroid cancers are slow tyrosine kinase inhibitor called pembrolizumab. Of the 6 growing and have an excellent prognosis, anaplastic patients that had surgery after this treatment, 4 patients thyroid cancer, which makes up <1% of all thyroid cancer, had the entire primary cancer removed and the other 2 is one of the most aggressive of all cancers, with a survival patients only had microscopic pieces of cancer left after averaging ~6 months after diagnosis. Surgery, radiation the surgery. After the surgery, 5 of 6 patients received and single drug chemotherapy is all ineffective in most standard chemotherapy and radiation to the surgical area. cases. The aim of this study is to study if combination Of the 6 patients, 4 patients had no evidence of cancer at chemotherapy will make previously inoperable anaplastic the last check, some over 2 years after surgery. The 2 other thyroid cancers safe to remove with surgery. patients did pass away from anaplastic cancer; however, there was no re-growth of cancer in the area where surgery THE FULL ARTICLE TITLE occurred. Wang JR et al 2019 Complete surgical resection following neoadjuvant dabrafenib plus trametinib in BRAFV600E- WHAT ARE THE IMPLICATIONS mutated anaplastic thyroid carcinoma. Thyroid 29:1036– OF THIS STUDY? 1043. PMID: 31319771. In selected patients with anaplastic thyroid cancer with the BRAF V600E mutation, treatment with dabrafenib SUMMARY OF THE STUDY and trametinib may increase the chance of having a In this study from the MD Anderson Cancer Center successful surgery of the primary tumor.
[Show full text]
Mutant Cancers 2 3 Heinz Hammerlindl1*, Dinoop Ravindran Menon1*, Sabrina Hammerlindl1, Abdullah Al
Author Manuscript Published OnlineFirst on December 1, 2017; DOI: 10.1158/1078-0432.CCR-16-2118 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Hammerlindl et. al 1 Acetylsalicylic Acid Governs the Effect of Sorafenib in RAS Mutant Cancers 2 3 Heinz Hammerlindl1*, Dinoop Ravindran Menon1*, Sabrina Hammerlindl1, Abdullah Al 4 Emran1, Joachim Torrano1, Katrin Sproesser3, Divya Thakkar1, Min Xiao3, Victoria G. 5 Atkinson5, Brian Gabrielli4, Nikolas K. Haass2, Meenhard Herlyn3, Clemens Krepler3, Helmut 6 Schaider1,2† 7 8 1Dermatology Research Centre, The University of Queensland, The University of 9 Queensland Diamantina Institute, Translational Research Institute, Brisbane, Australia; 10 2The University of Queensland, The University of Queensland Diamantina Institute, 11 Translational Research Institute, Brisbane, Australia; 12 3The Wistar Institute, Philadelphia, PA, U.S.A.; 13 4Mater Medical Research Institute, The University of Queensland, Translational Research 14 Institute, Brisbane, Australia; 15 5Division of Cancer Services, Princess Alexandra Hospital, Brisbane, Australia; 16 *These authors contributed equally to the study 17 18 Running title: 19 Combined aspirin and sorafenib for RAS-mutant cancer therapy 20 21 Key words: 22 Melanoma, Lung Cancer, NRAS, Sorafenib, Aspirin, RAS, ERK, AMPK 23 24 25 26 27 28 1 Downloaded from clincancerres.aacrjournals.org on September 24, 2021. © 2017 American Association for Cancer Research. Author Manuscript Published OnlineFirst on December 1, 2017; DOI: 10.1158/1078-0432.CCR-16-2118 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Hammerlindl et. al 1 2 Grant Support 3 This work was funded by the Epiderm Foundation (H.S.), the Princess Alexandra Hospital 4 Research Foundation (PARSS2016_NearMiss) (H.S.), NIH grants PO1 CA114046, P50 5 CA174523, and the Dr.
[Show full text]
Center for Drug Evaluation and Research
CENTER FOR DRUG EVALUATION AND RESEARCH Approval Package for: APPLICATION NUMBER: 125554Origs051 Trade Name: OPDIVO Generic or Proper nivolumab Name: Sponsor: Bristol-Myers Squibb Company Approval Date: March 05, 2018 Indication: Opdivo is a programmed death receptor-1 (PD-1) blocking antibody indicated for the treatment of: • patients with BRAF V600 wild-type unresectable or metastatic melanoma, as a single agent. (1.1) • patients with BRAF V600 mutation-positive unresectable or metastatic melanoma, as a single agent.a (1.1) • patients with unresectable or metastatic melanoma, in combination with ipilimumab.a (1.1) • patients with melanoma with lymph node involvement or metastatic disease who have undergone complete resection, in the adjuvant setting. (1.2) • patients with metastatic non-small cell lung cancer and progression on or after platinum-based chemotherapy. Patients with EGFT or ALK genomic tumor aberrations should have disease progression on FDA-approved therapy for these aberrations prior to receiving OPDIVO. (1.3) • patients with advanced renal cell carcinoma who have received prior anti-angiogenic therapy. (1.4) • adult patients with classical Hodgkin lymphoma that has relapsed or progressed afterb: (1.5) o autologous hematopoietic stem cell transplantation (HSCT) and brentuximab vedotin, or o 3 or more lines of systemic therapy that includes autologous HSCT. • patients with recurrent or metastatic squamous cell carcinoma of the head and neck with disease progression on or after a platinum-based therapy (1.6) • patients with locally advanced or metastatic urothelial carcinoma whob: o have disease progression during or following platinum-containing chemotherapy o have disease progression within 12 months of neoadjuvant or adjuvant treatment with platinum- containing chemotherapy.
[Show full text]
New Oncology Reimbursements in Belgium
33 New oncology reimbursements in Belgium P. Specenier, MD, PhD OVERVIEW OF BELGIAN REIMBURSEMENT NEWS (BELG J MED ONCOL 2018;12(1):33-34) TEMOZOLOMIDE® (TEMODAR/TEMODAL) was 7.4 months (95% confidence interval [CI] 5.6-9.1) with Some companies have transferred temozolomide from chap- cabozantinib versus 3.8 months (95% CI 3.7-5.4) with ever- ter IV to chapter I. These can now be prescribed without re- olimus with a hazard ratio (HR) of 0.58 (95% CI 0.45-0.74; strictions. In the near future, other temozolomide brands are p<0.0001). Similar data were observed in the intent-to-treat also expected to be transferred. population. A planned interim analysis of overall survival (OS) was conducted at the time of the PFS analysis and did LOMUSTINE (CCNU) not reach the interim boundary for statistical significance The reimbursement criteria for lomustine have been modi- (HR=0.68 [0.51, 0.90], p=0.006). However, in a subsequent fied and are entirely concordant with the recently modified unplanned interim analysis of OS, a statistically significant criteria for procarbazine, except for the indication Hodgkin’s improvement was demonstrated (median 21.4 months ver- disease, which only applies for procarbazine. sus 16.5 months; HR=0.66; 95% CI 0.53-0.83; p=0.0003). The overall response rate (ORR) was 17% (95% CI 13-22) for CABOMETYX® (CABOZANTINIB) cabozantinib and 3% (95% CI 2-6) for everolimus (p<0.0001). Cabometyx® (cabozantinib) can be reimbursed for patients with advanced renal cell carcinoma (RCC) after at least one COTELLIC® (COBIMETINIB) prior anti-VEGF directed agent.
[Show full text]
Combined BRAF and MEK Inhibition with Vemurafenib and Cobimetinib for Patients with Advanced Melanoma
Review Melanoma Combined BRAF and MEK Inhibition with Vemurafenib and Cobimetinib for Patients with Advanced Melanoma Antonio M Grimaldi, Ester Simeone, Lucia Festino, Vito Vanella and Paolo A Ascierto Melanoma, Cancer Immunotherapy and Innovative Therapy Unit, Istituto Nazionale Tumori Fondazione “G. Pascale”, Napoli, Italy cquired resistance is the most common cause of BRAF inhibitor monotherapy treatment failure, with the majority of patients experiencing disease progression with a median progression-free survival of 6-8 months. As such, there has been considerable A focus on combined therapy with dual BRAF and MEK inhibition as a means to improve outcomes compared with monotherapy. In the COMBI-d and COMBI-v trials, combined dabrafenib and trametinib was associated with significant improvements in outcomes compared with dabrafenib or vemurafenib monotherapy, in patients with BRAF-mutant metastatic melanoma. The combination of vemurafenib and cobimetinib has also been investigated. In the phase III CoBRIM study in patients with unresectable stage III-IV BRAF-mutant melanoma, treatment with vemurafenib and cobimetinib resulted in significantly longer progression-free survival and overall survival (OS) compared with vemurafenib alone. One-year OS was 74.5% in the vemurafenib and cobimetinib group and 63.8% in the vemurafenib group, while 2-year OS rates were 48.3% and 38.0%, respectively. The combination was also well tolerated, with a lower incidence of cutaneous squamous-cell carcinoma and keratoacanthoma compared with monotherapy. Dual inhibition of both MEK and BRAF appears to provide a more potent and durable anti-tumour effect than BRAF monotherapy, helping to prevent acquired resistance as well as decreasing adverse events related to BRAF inhibitor-induced activation of the MAPK-pathway.
[Show full text]
Original Research Paper In-Silico FDA-Approved Drug Repurposing to Find
Original Research Paper In-silico FDA-approved drug repurposing to find the possible treatment of Coronavirus Disease-19 (COVID-19) Kumar Sharp1, Dr. Shubhangi Dange2* 12nd MBBS undergraduate student, Government Medical College and Hospital, Jalgaon 2Associate Professor, Dept. of Microbiology, Government Medical College and Hospital, Jalgaon *Corresponding author: - Dr. Shubhangi Dange, Associate Professor, Department of Microbiology, Government Medical College and Hospital, Jalgaon Email: [email protected] Abstract Identification of potential drug-target interaction for approved drugs serves as the basis of repurposing drugs. Studies have shown polypharmacology as common phenomenon. In-silico approaches help in screening large compound libraries at once which could take years in a laboratory. We screened a library of 1050 FDA-approved drugs against spike glycoprotein of SARS-CoV2 in-silico. Anti-cancer drugs have shown good binding affinity which is much better than hydroxychloroquine and arbidol. We have also introduced a hypothesis named “Bump” hypothesis which and be developed further in field of computational biology. Keywords: spike glycoprotein; FDA; drug repurposing; anti-cancer; hydroxychloroquine Introduction Identification of potential drug-target interaction for approved drugs serves as the basis of repurposing drugs. Studies have shown polypharmacology as common phenomenon [1][2]. Since the three-dimensional structures of proteins of SARS-CoV2 have been mapped it opens opportunity for in-silico approaches of either novel drug discovery or drug repurposing. In the absence of an exact cure or vaccine, coronavirus disease-19 has taken a huge toll of humanity. Our study of target specific drug docking and novel hypothesis contributes in this fight. In-silico approaches help in screening large compound libraries at once which could take years in a laboratory.
[Show full text]