Colorectal and Gastric Cancer (Faculty Presentations)

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POST-TEST Recent Advances in Medical Oncology: Colorectal and Gastric Cancer (Faculty Presentations) THE CORRECT ANSWER IS INDICATED WITH YELLOW HIGHLIGHTING. 1. Which combination regimen recently 4. Which type of agent is zanidatamab received FDA approval on the basis of (ZW25), an investigational drug that has results from the BEACON CRC trial yielded promising responses in patients evaluating encorafenib/cetuximab with with heavily pretreated biliary, colorectal or without binimetinib versus investiga- and gastroesophageal cancer? tor’s choice of irinotecan/cetuximab or a. Anti-PD-1/PD-L1 antibody FOLFIRI/cetuximab for patients with b. Angiogenesis inhibitor metastatic colorectal cancer (mCRC) c. Cancer cell stemness inhibitor with BRAF V600E mutations? d. Bispecific antibody against HER2 a. Encorafenib/cetuximab/binimetinib only 5. Which of the following patients with RAS b. Encorafenib/cetuximab only wild-type mCRC derive clinical benefit c. Encorafenib/cetuximab and from the addition of EGFR antibodies to encorafenib/cetuximab/binimetinib first-line chemotherapy? a. Patients with left-sided primary 2. Which of the following drug descriptions disease best reflects the mechanism of action of b. Patients with right-sided primary trastuzumab deruxtecan? disease a. Immune checkpoint inhibitor b. Antibody-drug conjugate 6. Which of the following CRC charac- c. Anti-VEGF receptor inhibitor teristics is predictive of benefit from treatment with immune checkpoint 3. Which of the following statements is inhibition (eg, pembrolizumab)? true about the promising results of the a. High microsatellite instability (MSI) ongoing Phase II DESTINY-CRC01 trial b. High tumor mutation burden investigating trastuzumab deruxtecan for c. Both a and b patients with unresectable or metastatic HER2-expressing CRC? d. Neither a nor b a. Responses were observed among 7. Which of the following is a common side only those patients who had previ- effect of TAS-102? ously received any HER2-directed therapy a. Hand-foot syndrome b. Responses were observed among b. Aphonia only those patients who had no c. Neutropenia prior exposure to HER2-directed therapy 8. Based on results of the KEYNOTE-177 trial, pembrolizumab is FDA approved for c. Responses were observed patients with mCRC in which setting? regardless of prior exposure to HER2-directed therapy a. As first-line therapy for patients with MSI-high disease b. As second-line therapy for patients with MSI-high disease c. As third- or later-line therapy for patients with microsatellite disease QID 2725 POST-TEST Recent Advances in Medical Oncology: Colorectal and Gastric Cancer (Faculty Presentations) THE CORRECT ANSWER IS INDICATED WITH YELLOW HIGHLIGHTING. 9. In the discovery cohort of the Circulating 10. The ongoing Phase III CanStem303C Cell-Free Genome Atlas Study, which of trial is evaluating which agent in combi- the following assays was established as nation with FOLFIRI with or without the best liquid-biopsy platform for early bevacizumab for previously treated detection of cancer? mCRC? a. Whole genome sequencing a. TAS-102 b. Targeted mutation assay b. Trastuzumab deruxtecan c. Methylation-based assay c. Encorafenib d. Napabucasin QID 2725.

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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.
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FOI Reference: FOI 414 - 2021
FOI Reference: FOI 414 - 2021 Title: Researching the Incidence and Treatment of Melanoma and Breast Cancer Date: February 2021 FOI Category: Pharmacy FOI Request: 1. How many patients are currently (in the past 3 months) undergoing treatment for melanoma, and how many of these are BRAF+? 2. In the past 3 months, how many melanoma patients (any stage) were treated with the following: • Cobimetinib • Dabrafenib • Dabrafenib AND Trametinib • Encorafenib AND Binimetinib • Ipilimumab • Ipilimumab AND Nivolumab • Nivolumab • Pembrolizumab • Trametinib • Vemurafenib • Vemurafenib AND Cobimetinib • Other active systemic anti-cancer therapy • Palliative care only 3. If possible, could you please provide the patients treated in the past 3 months with the following therapies for metastatic melanoma ONLY: • Ipilimumab • Ipilimumab AND Nivolumab • Nivolumab • Pembrolizumab • Any other therapies 4. In the past 3 months how many patients were treated with the following for breast cancer? • Abemaciclib + Anastrozole/Exemestane/Letrozole • Abemaciclib + Fulvestrant • Alpelisib + Fulvestrant • Atezolizumab • Bevacizumab [Type text] • Eribulin • Everolimus + Exemestane • Fulvestrant as a single agent • Gemcitabine + Paclitaxel • Lapatinib • Neratinib • Olaparib • Palbociclib + Anastrozole/Exemestane/Letrozole • Palbociclib + Fulvestrant • Pertuzumab + Trastuzumab + Docetaxel • Ribociclib + Anastrozole/Exemestane/Letrozole • Ribociclib + Fulvestrant • Talazoparib • Transtuzumab + Paclitaxel • Transtuzumab as a single agent • Trastuzumab emtansine • Any other
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Summary Risk Management Plan for Braftovi
Summary of the risk management plan Summary of the risk management plan for BRAFTOVI This is a summary of the risk management plan (RMP) for BRAFTOVI when administered in combination with MEKTOVI or cetuximab. The RMP details important risks of BRAFTOVI in combination with MEKTOVI or cetuximab, how these risks can be minimised, and how more information will be obtained about BRAFTOVI in combination with MEKTOVI or cetuximab risks and uncertainties (missing information). Summary of product characteristics (SmPC) for BRAFTOVI and its package leaflets give essential information to healthcare professionals and patients on how BRAFTOVI should be used. This summary of the RMP for BRAFTOVI when administered in combination with MEKTOVI or cetuximab should be read in the context of all this information including the assessment reports of the evaluation and the plain-language summary, all of which are part of the European Public Assessment Report (EPAR). Important new concerns or changes to current concerns will be included in future updates of the RMP for BRAFTOVI. I. The medicine and what it is used for BRAFTOVI is authorised in combination with MEKTOVI for the treatment of adult patients with unresectable or metastatic melanoma with a BRAF V600 mutation (see SmPC for the full indication). The active substance of BRAFTOVI is encorafenib and of MEKTOVI is binimetinib and both are given by the oral route of administration. BRAFTOVI in combination with cetuximab is authorised for the treatment of adult patients with metastatic colorectal cancer (CRC) with a BRAF V600E mutation, who have received prior systemic therapy. Cetuximab is given by intravenous infusion.
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In This Issue
IN THIS ISSUE The HER2T798I Mutation Promotes Acquired Resistance to Neratinib • A patient with breast cancer • HER2T798I acquisition promoted • Patients with HER2L869R/T798I tumors harboring the HER2L869R mutation neratinib resistance, but cells remained may respond to afatinib even after initially responded to neratinib. sensitive to afatinib in vitro. neratinib resistance develops. The receptor tyrosine kinase Consistent with these findings, HER2L869R expression trans- HER2 (also known as ERBB2) is formed MCF10A breast epithelial cells, and neratinib blocked subject to activating mutations the activity of HER2L869R. Based on these findings, the patient in a subset of breast cancers. was enrolled in a clinical trial to receive single-agent neratinib Irreversible EGFR/HER2 tyros- and exhibited an excellent clinical response. The patient even- ine kinase inhibitors includ- tually progressed on neratinib, and NGS detected an acquired ing neratinib and afatinib have HER2T798I mutation. Computational models predicted that demonstrated preclinical activity this mutation would result in steric hindrance to reduce ner- against HER2-mutant tumors atinib binding. Indeed, the T798I mutation reduced HER2 and clinical trials are ongoing. stability and rendered HER2L869R-transformed cells refrac- Hanker and colleagues identified aHER2 kinase domain tory to neratinib, suggesting that neratinib treatment selects mutation (HER2L869R) in a patient with estrogen receptor– for the HER2T798I mutation to promote neratinib resistance. positive, progesterone receptor–positive lobular breast carci- HER2L869R/T798I cells that had developed resistance to ner- noma through targeted capture next-generation sequencing atinib showed sensitivity to afatinib. In addition to identify- (NGS) of DNA from a skin metastasis. Structural modeling ing HER2T798I as an acquired neratinib-resistant mutation, predicted that the HER2L869R mutation would destabilize the these results suggest that patients with this mutation may inactive kinase conformation to activate HER2.
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Comparator Report on Cancer in Europe 2019 −Disease Burden, Costs and Access to Medicines
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BRAFTOVI (Encorafenib) RATIONALE for INCLUSION in PA PROGRAM
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