Alunbrig (Brigatinib)

Total Page：16

File Type：pdf, Size：1020Kb

Alunbrig® (brigatinib) – Expanded indication • On May 22, 2020, Takeda announced the FDA approval of Alunbrig (brigatinib), for the treatment of adult patients with anaplastic lymphoma kinase (ALK)-positive metastatic non-small cell lung cancer (NSCLC) as detected by an FDA-approved test. — Alunbrig was previously approved for the treatment of patients with ALK-positive metastatic NSCLC who have progressed on or are intolerant to Xalkori® (crizotinib). • This approval expands Alunbrig’s indication to include the first-line setting. • The approval of Alunbrig for the expanded indication was based on the ALTA 1L trial, a randomized, open-label study in 275 adult patients with advanced ALK-positive NSCLC who had not previously received an ALK-targeted therapy. Patients were randomized to receive Alunbrig or Xalkori. The major efficacy outcome measure was progression-free survival (PFS) and additional efficacy outcome measures included confirmed overall response rate (ORR) and duration of response (DOR). — Median PFS was 24.0 months vs. 11.0 months for Alunbrig and Xalkori, respectively (hazard ratio [HR] 0.49; 95% CI: 0.35, 0.68; p < 0.0001). — The confirmed ORR was 74% (95% CI: 66, 81) for Alunbrig vs. 62% (95% CI: 53, 70) for Xalkori (p = 0.0342). — The median DOR was not reached (95% CI: 19.4, not estimable) for Alunbrig and 13.8 months (95% CI: 9.3, 20.8) for Xalkori. • The recommended dose of Alunbrig is 90 mg orally once daily for the first 7 days; then the dose should be increased to 180 mg orally once daily. Alunbrig should be administered until disease progression or unacceptable toxicity. — Patients should be selected for the treatment based on the presence of ALK positivity in tumor specimens. Information on FDA-approved tests for the detection of ALK rearrangements in NSCLC is available at http://www.fda.gov/CompanionDiagnostics. optumrx.com OptumRx® specializes in the delivery, clinical management and affordability of prescription medications and consumer health products. We are an Optum® company — a leading provider of integrated health services. Learn more at optum.com. All Optum® trademarks and logos are owned by Optum, Inc. All other brand or product names are trademarks or registered marks of their respective owners. This document contains information that is considered proprietary to OptumRx and should not be reproduced without the express written consent of OptumRx. RxNews® is published by the OptumRx Clinical Services Department. ©2020 Optum, Inc. All rights reserved. .

Copy Link

Recommended publications

New Drug Update: the Next Step in Personalized Medicine
New Drug Update: The Next Step in Personalized Medicine Jordan Hill, PharmD, BCOP Clinical Pharmacy Specialist WVU Medicine Mary Babb Randolph Cancer Center Objectives • Review indications for new FDA approved anti- neoplastic medications in 2017 • Outline place in therapy of new medications • Become familiar with mechanisms of action of new medications • Describe adverse effects associated with new medications • Summarize dosing schemes and appropriate dose reductions for new medications First-in-Class Approvals • FLT3 inhibitor – midostaurin • IDH2 inhibitor – enasidenib • Anti-CD22 antibody drug conjugate – inotuzumab ozogamicin • CAR T-cell therapy - tisagenlecleucel “Me-too” Approvals • CDK 4/6 inhibitor – ribociclib and abemaciclib • PD-L1 inhibitors • Avelumab • Durvalumab • PARP inhibitor – niraparib • ALK inhibitor – brigatinib • Pan-HER inhibitor – neratinib • Liposome-encapsulated combination of daunorubicin and cytarabine • PI3K inhibitor – copanlisib Drugs by Malignancy AML Breast Bladder ALL FL Lung Ovarian 0 1 2 3 Oral versus IV 46% 54% Oral IV FIRST-IN CLASS FLT3 Inhibitor - midostaurin Journal of Hematology & Oncology 2017;10:93 Midostaurin (Rydapt®) • 717 newly diagnosed FLT3+ AML Patients • Induction and consolidation chemotherapy and placebo maintenance versus chemotherapy + midostaurin and Treatment maintenance midostaurin • OS: 74.7 mo versus 25.6 mo (P=0.009) Efficacy • EFS: 8.2 mo versus 3.0 mo (P=0.002) • Higher grade > 3 anemia, rash, and nausea Safety N Engl J Med 2017;377:454-64 Midostaurin (Rydapt®) • Approved indications: FLT3+ AML, mast cell leukemia, systemic mastocytosis • AML dose: 50 mg twice daily with food on days 8-21 • Of each induction cycle (+ daunorubicin and cytarabine) • Of each consolidation cycle (+ high dose cytarabine) • ADEs: nausea, myelosuppression, mucositis, increases in LFTs, amylase/lipase, and electrolyte abnormalities • Pharmacokinetics: hepatic metabolism, substrate of CYP 3A4; < 5% excretion in urine RYDAPT (midostaurin) [package insert].
[Show full text]
First-Line Treatment Options for Patients with Stage IV Non-Small Cell Lung Cancer with Driver Alterations
First-Line Treatment Options for Patients with Stage IV Non-Small Cell Lung Cancer with Driver Alterations Patients with stage IV non-small cell lung cancer Nonsquamous cell carcinoma and squamous cell carcinoma Activating EGFR mutation other Sensitizing (L858R/exon 19 MET exon 14 skipping than exon 20 insertion mutations, EGFR exon 20 mutation ALK rearrangement ROS1 rearrangement BRAF V600E mutation RET rearrangement NTRK rearrangement mutations KRAS alterations HER2 alterations NRG1 alterations deletion) EGFR mutation T790M, L858R or Ex19Del PS 0-2 Treatment Options PS 0-2 Treatment Options PS 0-2 Treatment Options PS 0-2 Treatment Options PS 0-2 Treatment Options Treatment Options PS 0-2 Treatment Options PS 0-2 Treatment Options PS 0-2 Treatment Options Emerging target; no Emerging target; no Emerging target; no Platinum doublet † † † Osimertinib monotherapy S Afatinib monotherapy M M Alectinib S Entrectinib M Dabrafenib/trametinib M Capmatinib M Selpercatinib M Entrectinib M conclusions available conclusions available conclusions available chemotherapy ± bevacizumab Gefitinib with doublet Standard treatment based on Standard treatment based on Standard treatment based on M M M Brigatinib S Crizotinib M M Tepotinib M Pralsetinib* W Larotrectinib M chemotherapy non-driver mutation guideline non-driver mutation guideline non-driver mutation guideline If alectinib or brigatinib are not available If entrectinib or crizotinib are not available Standard treatment based on Standard treatment based on Standard treatment based on Dacomitinib monotherapy M Osimertinib W M M M Ceritinib S Ceritinib W non-driver mutation guideline non-driver mutation guideline non-driver mutation guideline Monotherapy with afatinib M Crizotinib S Lortlatinib W Standard treatment based on Erlotinib/ramucirumab M M non-driver mutation guideline Erlotinib/bevacizumab M Monotherapy with erlotinib M Strength of Recommendation Monotherapy with gefitinib M S Strong M Moderate W Weak Monotherapy with icotinib M Notes.
[Show full text]
Newer-Generation EGFR Inhibitors in Lung Cancer: How Are They Best Used?
cancers Review Newer-Generation EGFR Inhibitors in Lung Cancer: How Are They Best Used? Tri Le 1 and David E. Gerber 1,2,3,* 1 Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390-8852, USA; [email protected] 2 Department of Clinical Sciences, University of Texas Southwestern Medical Center, Dallas, TX 75390-8852, USA 3 Division of Hematology-Oncology, Harold C. Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75390-8852, USA * Correspondence: [email protected]; Tel.: +1-214-648-4180; Fax: +1-214-648-1955 Received: 15 January 2019; Accepted: 4 March 2019; Published: 15 March 2019 Abstract: The FLAURA trial established osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), as a viable first-line therapy in non-small cell lung cancer (NSCLC) with sensitizing EGFR mutations, namely exon 19 deletion and L858R. In this phase 3 randomized, controlled, double-blind trial of treatment-naïve patients with EGFR mutant NSCLC, osimertinib was compared to standard-of-care EGFR TKIs (i.e., erlotinib or gefinitib) in the first-line setting. Osimertinib demonstrated improvement in median progression-free survival (18.9 months vs. 10.2 months; hazard ratio 0.46; 95% CI, 0.37 to 0.57; p < 0.001) and a more favorable toxicity profile due to its lower affinity for wild-type EGFR. Furthermore, similar to later-generation anaplastic lymphoma kinase (ALK) inhibitors, osimertinib has improved efficacy against brain metastases. Despite this impressive effect, the optimal sequencing of osimertinib, whether in the first line or as subsequent therapy after the failure of earlier-generation EGFR TKIs, is not clear.
[Show full text]
Brigatinib Combined with Anti-EGFR Antibody Overcomes Osimertinib Resistance in EGFR-Mutated Non-Small-Cell Lung Cancer
ARTICLE Received 29 Sep 2016 | Accepted 30 Jan 2017 | Published 13 Mar 2017 DOI: 10.1038/ncomms14768 OPEN Brigatinib combined with anti-EGFR antibody overcomes osimertinib resistance in EGFR-mutated non-small-cell lung cancer Ken Uchibori1,2, Naohiko Inase2, Mitsugu Araki3, Mayumi Kamada4, Shigeo Sato1, Yasushi Okuno3,4, Naoya Fujita1 & Ryohei Katayama1 Osimertinib has been demonstrated to overcome the epidermal growth factor receptor (EGFR)-T790M, the most relevant acquired resistance to first-generation EGFR–tyrosine kinase inhibitors (EGFR–TKIs). However, the C797S mutation, which impairs the covalent binding between the cysteine residue at position 797 of EGFR and osimertinib, induces resistance to osimertinib. Currently, there are no effective therapeutic strategies to overcome the C797S/T790M/activating-mutation (triple-mutation)-mediated EGFR–TKI resistance. In the present study, we identify brigatinib to be effective against triple-mutation-harbouring cells in vitro and in vivo. Our original computational simulation demonstrates that brigatinib fits into the ATP-binding pocket of triple-mutant EGFR. The structure–activity relationship analysis reveals the key component in brigatinib to inhibit the triple-mutant EGFR. The efficacy of brigatinib is enhanced markedly by combination with anti-EGFR antibody because of the decrease of surface and total EGFR expression. Thus, the combination therapy of brigatinib with anti-EGFR antibody is a powerful candidate to overcome triple-mutant EGFR. 1 Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto-ku, Tokyo 135-8550, Japan. 2 Department of Respiratory Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Japan.
[Show full text]
Estimation of the Percentage of US Patients with Cancer Who Benefit from Genome‐Driven Oncology
Supplementary Online Content Marquart J, Chen EY, Prasad V. Estimation of the percentage of US patients with cancer who benefit from genome‐driven oncology. JAMA Oncology. Published online April 17, 2018. doi:10.1001/jamaoncol.2018.1660 eAppendix 1. Yearly Cancer Statistics eAppendix 2. Data Sources by Malignancy eAppendix 3. Pie Charts Estimating Patients Eligible for Genomically Targeted Therapy eAppendix 4. Pie Charts Estimating Patients Who Could Benefit from Genomically Targeted Therapy eAppendix 5. Pie Charts Estimating Patients Eligible for Genomically Informed Therapy eAppendix 6. Pie Charts Estimating Patients Who Could Benefit from Genomically Informed Therapy eAppendix 7. Pie Charts Estimating Patients Eligible for and who could Benefit from Adjuvant Therapy eFigure 1. Percent of US metastatic Cancer Patients Who May be Eligible for and Benefit from Genomically Informed Treatment eFigure 2. Growth of Genome Targeted and Informed Therapy Over Time With Fitted Linear Regression This supplementary material has been provided by the authors to give readers additional information about their work. 1 © 2018 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/27/2021 eAppendix 1. Cancer Statistics by Year: 2006: https://www.ncbi.nlm.nih.gov/pubmed/16514137 2007: https://www-ncbi-nlm-nih-gov/pubmed/17237035 2008: https://www-ncbi-nlm-nih-gov/pubmed/18287387 2009: https://www-ncbi-nlm-nih-gov/pubmed/19474385 2010: https://www-ncbi-nlm-nih-gov/pubmed/20610543 2011: https://www.ncbi.nlm.nih.gov/pubmed/21685461 2012: https://www.ncbi.nlm.nih.gov/pubmed/22237781 2013: https://www.ncbi.nlm.nih.gov/pubmed/23335087 2014: https://www.ncbi.nlm.nih.gov/pubmed/24890451 2015: https://www.ncbi.nlm.nih.gov/pubmed/25559415 2016: https://www.ncbi.nlm.nih.gov/pubmed/26742998 2017: https://www.ncbi.nlm.nih.gov/pubmed/28055103 2018: https://www.ncbi.nlm.nih.gov/pubmed/29313949 eAppendix 2.
[Show full text]
Oncology Oral, Lung Cancer Therapeutic Class Review (TCR)
Oncology Oral, Lung Cancer Therapeutic Class Review (TCR) April 14, 2020 No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, digital scanning, or via any information storage or retrieval system without the express written consent of Magellan Rx Management. All requests for permission should be mailed to: Magellan Rx Management Attention: Legal Department 6950 Columbia Gateway Drive Columbia, Maryland 21046 The materials contained herein represent the opinions of the collective authors and editors and should not be construed to be the official representation of any professional organization or group, any state Pharmacy and Therapeutics committee, any state Medicaid Agency, or any other clinical committee. This material is not intended to be relied upon as medical advice for specific medical cases and nothing contained herein should be relied upon by any patient, medical professional or layperson seeking information about a specific course of treatment for a specific medical condition. All readers of this material are responsible for independently obtaining medical advice and guidance from their own physician and/or other medical professional in regard to the best course of treatment for their specific medical condition. This publication, inclusive of all forms contained herein, is intended to be educational in nature and is intended to be used for informational purposes only. Send comments and suggestions to [email protected]. April 2020 Proprietary Information. Restricted Access – Do not disseminate or copy without approval. © 2010–2020 Magellan Rx Management. All rights reserved. FDA-APPROVED INDICATIONS Drug Manufacturer Indication(s) Anaplastic Lymphoma Kinase (ALK) Tyrosine Kinase Inhibitors alectinib Genentech .
[Show full text]
The New-Generation Selective ROS1/NTRK Inhibitor DS-6051B Overcomes Crizotinib Resistant ROS1- G2032R Mutation in Preclinical Models
ARTICLE https://doi.org/10.1038/s41467-019-11496-z OPEN The new-generation selective ROS1/NTRK inhibitor DS-6051b overcomes crizotinib resistant ROS1- G2032R mutation in preclinical models Ryohei Katayama 1, Bo Gong1,2, Noriko Togashi 3, Masaya Miyamoto3, Masaki Kiga3, Shiho Iwasaki3, Yasuki Kamai3, Yuichi Tominaga3, Yasuyuki Takeda3, Yoshiko Kagoshima3, Yuki Shimizu1,2, Yosuke Seto1, Tomoko Oh-hara1, Sumie Koike1, Naoki Nakao4, Hiroyuki Hanzawa4, Kengo Watanabe 3, Satoshi Yoda 5,6, Noriko Yanagitani7, Aaron N. Hata5,6, Alice T. Shaw5,6, Makoto Nishio7, Naoya Fujita1,2 & Takeshi Isoyama 3 1234567890():,; ROS1 gene rearrangement was observed in around 1–2 % of NSCLC patients and in several other cancers such as cholangiocarcinoma, glioblastoma, or colorectal cancer. Crizotinib, an ALK/ROS1/MET inhibitor, is highly effective against ROS1-rearranged lung cancer and is used in clinic. However, crizotinib resistance is an emerging issue, and several resistance mechanisms, such as secondary kinase-domain mutations (e.g., ROS1-G2032R) have been identiﬁed in crizotinib-refractory patients. Here we characterize a new selective ROS1/NTRK inhibitor, DS-6051b, in preclinical models of ROS1- or NTRK-rearranged cancers. DS-6051b induces dramatic growth inhibition of both wild type and G2032R mutant ROS1–rearranged cancers or NTRK-rearranged cancers in vitro and in vivo. Here we report that DS-6051b is effective in treating ROS1- or NTRK-rearranged cancer in preclinical models, including crizotinib-resistant ROS1 positive cancer with secondary kinase domain mutations especially G2032R mutation which is highly resistant to crizotinib as well as lorlatinib and entrectinib, next generation ROS1 inhibitors. 1 Division of Experimental Chemotherapy, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo 135-8550, Japan.
[Show full text]
Focus on ROS1-Positive Non-Small Cell Lung Cancer (NSCLC): Crizotinib, Resistance Mechanisms and the Newer Generation of Targeted Therapies
cancers Review Focus on ROS1-Positive Non-Small Cell Lung Cancer (NSCLC): Crizotinib, Resistance Mechanisms and the Newer Generation of Targeted Therapies Alberto D’Angelo 1,* , Navid Sobhani 2 , Robert Chapman 3 , Stefan Bagby 1, Carlotta Bortoletti 4, Mirko Traversini 5, Katia Ferrari 6, Luca Voltolini 7, Jacob Darlow 1 and Giandomenico Roviello 8 1 Department of Biology and Biochemistry, University of Bath, Bath BA2 7AY, UK; [email protected] (S.B.); [email protected] (J.D.) 2 Section of Epidemiology and Population Science, Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA; [email protected] 3 University College London Hospitals NHS Foundation Trust, 235 Euston Rd, London NW1 2BU, UK; [email protected] 4 Department of Dermatology, University of Padova, via Vincenzo Gallucci 4, 35121 Padova, Italy; [email protected] 5 Unità Operativa Anatomia Patologica, Ospedale Maggiore Carlo Alberto Pizzardi, AUSL Bologna, Largo Bartolo Nigrisoli 2, 40100 Bologna, Italy; [email protected] 6 Respiratory Medicine, Careggi University Hospital, 50139 Florence, Italy; [email protected] 7 Thoracic Surgery Unit, Careggi University Hospital, Largo Brambilla, 1, 50134 Florence, Italy; luca.voltolini@uniﬁ.it 8 Department of Health Sciences, Section of Clinical Pharmacology and Oncology, University of Florence, Viale Pieraccini, 6, 50139 Florence, Italy; [email protected] * Correspondence: [email protected] Received: 22 September 2020; Accepted: 5 November 2020; Published: 6 November 2020 Simple Summary: Genetic rearrangements of the ROS1 gene account for up to 2% of NSCLC patients who sometimes develop brain metastasis, resulting in poor prognosis. This review discusses the tyrosine kinase inhibitor crizotinib plus updates and preliminary results with the newer generation of tyrosine kinase inhibitors, which have been speciﬁcally conceived to overcome crizotinib resistance, including brigatinib, cabozantinib, ceritinib, entrectinib, lorlatinib and repotrectinib.
[Show full text]
Unitedhealthcare Cancer Therapy Pathways Program Regimens
UnitedHealthcare Cancer Therapy Pathways Program Overview 2 Breast Cancer 3 Pancreatic Cancer 15 Melanoma 19 Colon/Rectal Cancer 23 Hepatobiliary Cancers 30 Lung Cancer, Small Cell 35 Lung Cancer, Non-Small Cell 40 Ovarian, Fallopian and Primary Peritoneal Cancer 56 Head and Neck Cancer 67 Multiple Myeloma 74 Lymphoma, Diffuse Large B-Cell 86 Lymphoma, Follicular 92 Lymphoma, Marginal Zone 97 Lymphoma, Mantle Cell 101 Change control 1 OVERVIEW Cancer Therapy Pathways Program With the rapid approval of new therapies, along with the rising cost of cancer care, pathways serve a critical role in the delivery of high-quality and high-value cancer treatments while reducing an unwarranted variation in care. The UnitedHealthcare Cancer Therapy Pathways Program aims to improve quality and value in cancer care by identifying anti-cancer regimens supported by evidence-based guidelines to help reduce total cost of care and improve outcomes. The program’s regimens are selected on the basis of clinical benefit (efficacy) and side-effect profile (toxicity). Among regimens with comparable efficacy and toxicity, additional consideration is given to the frequency of hospitalizations during therapy, duration of therapy, drug costs and total cost of care. Care decisions are between the physician and the patient The Cancer Therapy Pathways Program is not a substitute for the experience and judgment of a physician or other health care professional. Any clinician participating in the program must use independent medical judgment in the context of individual
[Show full text]
Kinase Drug Discovery 20 Years After Imatinib: Progress and Future Directions
REVIEWS Kinase drug discovery 20 years after imatinib: progress and future directions Philip Cohen 1 ✉ , Darren Cross 2 ✉ and Pasi A. Jänne 3 ✉ Abstract | Protein kinases regulate nearly all aspects of cell life, and alterations in their expression, or mutations in their genes, cause cancer and other diseases. Here, we review the remarkable progress made over the past 20 years in improving the potency and specificity of small-molecule inhibitors of protein and lipid kinases, resulting in the approval of more than 70 new drugs since imatinib was approved in 2001. These compounds have had a significant impact on the way in which we now treat cancers and non- cancerous conditions. We discuss how the challenge of drug resistance to kinase inhibitors is being met and the future of kinase drug discovery. Protein kinases In 2001, the first kinase inhibitor, imatinib, received FDA entered clinical trials in 1998, changed the perception Enzymes that catalyse transfer approval, providing the catalyst for an article with the of protein kinases as drug targets, which had previously of the γ- phosphate of ATP provocative title ‘Protein kinases — the major drug tar- received scepticism from many pharmaceutical com- to amino acid side chains in gets of the twenty- first century?’1. Imatinib inhibits the panies. Since then, hundreds of protein kinase inhibi- substrate proteins, such as serine, threonine and tyrosine Abelson (ABL) tyrosine kinase, which is expressed as a tors have been developed and tested in humans and, at residues. deregulated fusion protein, termed BCR–ABL, in nearly the time of writing, 76 have been approved for clinical all cases of chronic myeloid leukaemia (CML)2 and is use, mainly for the treatment of various cancers (FiG.
[Show full text]
The Emerging Therapeutic Landscape of ALK Inhibitors in Non-Small Cell Lung Cancer
pharmaceuticals Review The Emerging Therapeutic Landscape of ALK Inhibitors in Non-Small Cell Lung Cancer 1, 1, 1, 1 Valerio Gristina y, Maria La Mantia y , Federica Iacono y, Antonio Galvano , 1, 2, , Antonio Russo z and Viviana Bazan * z 1 Department of Surgical, Oncological and Oral Sciences, University of Palermo, 90127 Palermo, Italy; [email protected] (V.G.); [email protected] (M.L.M.); [email protected] (F.I.); [email protected] (A.G.); [email protected] (A.R.) 2 Department of Biomedicine, Neuroscience and Advanced Diagnostics (Bi.N.D.), Section of Medical Oncology, University of Palermo, 90127 Palermo, Italy * Correspondence: [email protected] These authors contributed equally to this work. y These authors are co-last. z Received: 29 October 2020; Accepted: 16 December 2020; Published: 18 December 2020 Abstract: The treatment of metastatic non-small cell lung cancer (NSCLC) has undergone a paradigm shift over the last decade. Better molecular characterization of the disease has led to the rapid improvement of personalized medicine and the prompt delivery of targeted therapies to patients with NSCLC. The discovery of the EML4-ALK fusion gene in a limited subset of patients aﬀected by NSCLC and the subsequent clinical development of crizotinib in 2011 has been an impressive milestone in lung cancer research. Unfortunately, acquired resistances regularly develop, hence disease progression occurs. Afterward, modern tyrosine kinase inhibitors (TKIs), such as ceritinib, alectinib, brigatinib, and lorlatinib, have been approved by the Food and Drug Administration (FDA) for the management of anaplastic lymphoma kinase (ALK)-positive NSCLCs.
[Show full text]
NCCN Guidelines for Central Nervous System Cancers V.1.2019 –Follow-Up Email Vote on 01/26/19
NCCN Guidelines for Central Nervous System Cancers V.1.2019 –Follow-Up Email Vote on 01/26/19 Guideline Page Panel Discussion/References Institution Vote and Request YES NO ABSTAIN ABSENT ASTR-1 Based on the data in the noted references, the panel consensus was to include 19 0 2 8 Internal request: Consider everolimus (as an example of an mTOR inhibitor) to be included as an adjuvant everolimus (as an example treatment option for patients with subependymal giant cell astrocytoma (SEGA). of an mTOR inhibitor) to be This is a category 2A recommendation. included as an adjuvant Franz DN, Belousova E, Sparagana S, et al. Everolimus for treatment option for subependymal giant cell astrocytoma in patients with tuberous sclerosis patients with subependymal complex: 2-year open-label extension of the randomised EXIST-1 study. giant cell astrocytoma Lancet Oncol 2014;15:1513-1520. (SEGA). Franz DN, Belousova E, Sparagana S, et al. Efficacy and safety of everolimus for subependymal giant cell astrocytomas associated with tuberous sclerosis complex (EXIST-1): a multicentre, randomised, placebo-controlled phase 3 trial. Lancet 2013;381:125-132. LEPT-2 The panel consensus was to include the changes to the treatment algorithms for 18 2 2 7 Internal request: Please leptomeningeal metastases. review the edits made to the treatment algorithms on this page for clarity. BRAIN-D (4 of 13) Based on the data in the noted reference, the panel consensus was to include 15 3 4 7 Internal request: lapatinib + temozolomide as a treatment option for progression of recurrent Should consideration of disease in patients with adult intracranial and/or spinal ependymoma.
[Show full text]