A Phase 1, Open-Label, 2-Part, Single Dose, Crossover Study to Examine the Effect of Food and Cobicistat Administration on the Pharmacokinetics and Safety of Plixorafenib in Healthy Participants.

The primary goal of this phase 1 study is to evaluate the effect of food and cobicistat on the pharmacokinetics of plixerafenib in healthy volunteers. Healthy male and female participants between the ages of 18 and 55 will be enrolled into this study. This study is looking to examine:
The effect of food on the single dose PK of plixorafenib administered with cobicistat.
The effect of cobicistat administration on the single dose PK of plixorafenib.
The safety of plixorafenib administered alone and with cobicistat in a single dose regimen in healthy participants.

Start Date24 Apr 2024

Sponsor / Collaborator

Fore Biotherapeutics, Inc.

NCT05503797 / RecruitingPhase 2

A Phase 2 Master Protocol to Assess the Efficacy and Safety of FORE8394, an Inhibitor of BRAF Class 1 and Class 2 Alterations, in Participants With Cancer Harboring BRAF Alterations

The objective of this study is to evaluate the efficacy of plixorafenib in participants with locally advanced or metastatic solid tumors, or recurrent or progressive primary central nervous system (CNS) tumors harboring BRAF fusions, or in participants with recurrent high-grade glioma (HGG) harboring BRAF V600E mutation. This will be conducted as two single arm open-label subprotocols (F8394-201A; F8394-201B) under one master protocol.

Start Date21 Feb 2023

Sponsor / Collaborator

Fore Biotherapeutics, Inc.

NCT02428712 / Active, not recruitingPhase 1/2

A Phase 1/2a Study to Assess the Safety, Pharmacokinetics, and Pharmacodynamics of FORE8394 in Patients With Advanced Unresectable Solid Tumors

The objective of this study is to determine the safety, pharmacokinetics, maximum tolerated dose/recommended Phase 2 dose, and efficacy of FORE8394.

Start Date01 Apr 2015

Sponsor / Collaborator

Fore Biotherapeutics, Inc.

100 Clinical Results associated with Plixorafenib

100 Translational Medicine associated with Plixorafenib

100 Patents (Medical) associated with Plixorafenib

Literatures (Medical) associated with Plixorafenib

01 Dec 2023·Oncogene

Inhibition of TGF-β signaling, invasion, and growth of cutaneous squamous cell carcinoma by PLX8394

Article

Author: Heino, Jyrki ; Nissinen, Liisa ; Riihilä, Pilvi ; Siljamäki, Elina ; Suwal, Ujjwal ; Rappu, Pekka ; Kähäri, Veli-Matti ; Kallajoki, Markku

Abstract:

Cutaneous squamous cell carcinoma (cSCC) is the most common metastatic skin cancer. The prognosis of patients with metastatic cSCC is poor emphasizing the need for new therapies. We have previously reported that the activation of Ras/MEK/ERK1/2 and transforming growth factor β (TGF-β)/Smad2 signaling in transformed keratinocytes and cSCC cells leads to increased accumulation of laminin-332 and accelerated invasion. Here, we show that the next-generation B-Raf inhibitor PLX8394 blocks TGF-β signaling in ras-transformed metastatic epidermal keratinocytes (RT3 cells) harboring wild-type B-Raf and hyperactive Ras. PLX8394 decreased phosphorylation of TGF-β receptor II and Smad2, as well as p38 activity, MMP-1 and MMP-13 synthesis, and laminin-332 accumulation. PLX8394 significantly inhibited the growth of human cSCC tumors and in vivo collagen degradation in xenograft model. In conclusion, our data indicate that PLX8394 inhibits several serine-threonine kinases in malignantly transformed human keratinocytes and cSCC cells and inhibits cSCC invasion and tumor growth in vitro and in vivo. We identify PLX8394 as a potential therapeutic compound for advanced human cSCC.

14 Jun 2023·Cell communication and signaling : CCS

Analysis of RAS and drug induced homo- and heterodimerization of RAF and KSR1 proteins in living cells using split Nanoluc luciferase.

Article

Author: Brummer, Tilman ; Rohrer, Lino ; Spohr, Corinna ; Braun, Sandra ; Beha, Carina ; Halbach, Sebastian ; Griffin, Ricarda

The dimerization of RAF kinases represents a key event in their activation cycle and in RAS/ERK pathway activation. Genetic, biochemical and structural approaches provided key insights into this process defining RAF signaling output and the clinical efficacy of RAF inhibitors (RAFi). However, methods reporting the dynamics of RAF dimerization in living cells and in real time are still in their infancy. Recently, split luciferase systems have been developed for the detection of protein-protein-interactions (PPIs), incl. proof-of-concept studies demonstrating the heterodimerization of the BRAF and RAF1 isoforms. Due to their small size, the Nanoluc luciferase moieties LgBiT and SmBiT, which reconstitute a light emitting holoenzyme upon fusion partner promoted interaction, appear as well-suited to study RAF dimerization. Here, we provide an extensive analysis of the suitability of the Nanoluc system to study the homo- and heterodimerization of BRAF, RAF1 and the related KSR1 pseudokinase. We show that KRAS^G12V promotes the homo- and heterodimerization of BRAF, while considerable KSR1 homo- and KSR1/BRAF heterodimerization already occurs in the absence of this active GTPase and requires a salt bridge between the CC-SAM domain of KSR1 and the BRAF-specific region. We demonstrate that loss-of-function mutations impairing key steps of the RAF activation cycle can be used as calibrators to gauge the dynamics of heterodimerization. This approach identified the RAS-binding domains and the C-terminal 14-3-3 binding motifs as particularly critical for the reconstitution of RAF mediated LgBiT/SmBiT reconstitution, while the dimer interface was less important for dimerization but essential for downstream signaling. We show for the first time that BRAF^V600E, the most common BRAF oncoprotein whose dimerization status is controversially portrayed in the literature, forms homodimers in living cells more efficiently than its wildtype counterpart. Of note, Nanoluc activity reconstituted by BRAF^V600E homodimers is highly sensitive to the paradox-breaking RAFi PLX8394, indicating a dynamic and specific PPI. We report the effects of eleven ERK pathway inhibitors on RAF dimerization, incl. third-generation compounds that are less-defined in terms of their dimer promoting abilities. We identify Naporafenib as a potent and long-lasting dimerizer and show that the split Nanoluc approach discriminates between type I, I^1/2 and II RAFi. Video Abstract.

01 Apr 2023·Virologica Sinica

PLX8394, a RAF inhibitor, inhibits enterovirus 71 replication by blocking RAF/MEK/ERK signaling

Article

Author: Huang, Chaolin ; Qiu, Fang ; Lin, Binbin ; Zhu, Guangyan ; Ren, Fuli ; Wu, Chengyuan ; Zhang, Dingyu ; Yang, Qingyu

Enterovirus 71 (EV71) poses a serious threat to human health, with scattered outbreaks worldwide. There are several vaccines against a few EV71 strains but no efficient drug for the treatment of EV71 infection. Therefore, it is urgent and of significance to develop anti-EV71 drugs. Here, we found that PLX8394, a RAF inhibitor, possesses high antiviral activity against EV71 in vitro, being superior to the traditional clinical drug ribavirin. Moreover, PLX8394 exhibits broad-spectrum antiviral activity against enteroviruses. Notably, in a suckling mouse model, PLX8394 provided a 70% protection rate for EV71-infected mice, reduced the viral load in liver and heart tissues, and relieved the inflammatory response. A mechanistic study showed that PLX8394 inhibited EV71 by suppressing the RAF/MEK/ERK signaling pathway. Thus, PLX8394 lays a foundation for the development of new drugs against EV71.

News (Medical) associated with Plixorafenib

09 Apr 2024

·www.biospace.com

FORE Biotherapeutics to Present Nonclinical Data at the 2024 AACR Annual Meeting Supporting Superior Potency for Plixorafenib Compared with BRAF or Pan-Raf Inhibitors, When Combined with MEK Inhibition

PHILADELPHIA--(BUSINESS WIRE)-- FORE Biotherapeutics today announced new nonclinical data related to plixorafenib (FORE8394; formerly PLX8394), the company's novel, investigational, small-molecule, next-generation, orally available selective inhibitor of BRAF alterations, will be presented at the AACR Annual Meeting 2024, taking place April 5-10, 2024, in San Diego and virtually. The data show nonclinical synergistic activity of plixorafenib when combined with MEK inhibition across all BRAF alterations tested. In cells with BRAF V600 or non-V600 mutations or BRAF fusions, the combination of plixorafenib and binimetinib is most potent of the BRAF and pan-RAF inhibitors tested. In plixorafenib resistant cells, these cells can be resensitized with the addition of binimetinib. To date, plixorafenib has demonstrated encouraging efficacy and safety data from the phase 1/2a study; these nonclinical data help build the foundation for potential future development of plixorafenib in combination with a MEK inhibitor. Poster Abstract number: 4609 Poster Title: The paradox-breaker BRAF inhibitor plixorafenib (PLX8394; FORE8394) synergizes with MEK inhibitors (MEKi) in BRAF V600 and non-V600 alterations, with higher potency compared to early generation BRAFi and pan-RAFi Presentation Session Date/Time: April 9, 2024, 9:00 AM - 12:30 PM Poster Session About Plixorafenib Plixorafenib is an investigational, novel, small-molecule, next-generation, orally available selective inhibitor of mutated BRAF. It was designed to target a wide range of BRAF alterations while sparing wild-type forms of RAF. Nonclinical and clinical studies have shown that its unique mechanism of action effectively inhibits not only the constitutively active BRAF V600 monomers targeted by first- and second-generation RAF inhibitors but also disrupts constitutively active dimeric BRAF class 2 mutants, fusions, splice variants and others. Unlike earlier-generation BRAF inhibitors, plixorafenib does not induce paradoxical activation of the RAF/MEK/ERK pathway. As a “paradox breaker”, plixorafenib could therefore address acquired resistance to current RAF inhibitors and, additionally, may yield improved safety and more durable efficacy than first-generation RAF inhibitors. Plixorafenib is currently being evaluated in two clinical trials in patients with advanced solid tumors with activating BRAF alterations. Interim clinical data from a Phase 1/2a trial presented at ESMO 2022, ASCO 2023 and SNO 2023 provided evidence of durable anti-tumor activity in patients with BRAF-mutated cancers with a 42% overall response rate and a median duration of response of 17.8 months in MAPK inhibitor-naïve participants with V600-mutated advanced solid tumors. Of the 9 patients with primary central nervous system tumors, 6 had confirmed response (ORR 67%) with a median duration of response of 13.9 months. In addition to the Phase 1/2a trial, plixorafenib is currently being investigated in the ongoing, potentially registrational Phase 2 FORTE study. About FORE Biotherapeutics Fore Bio is a precision oncology company dedicated to developing innovative treatments that provide better outcomes for patients with the hardest-to-treat cancers. The Company’s lead asset plixorafenib (FORE8394; formerly PLX8394) is a V600 and non-V600 BRAF inhibitor with manageable clinical safety and early efficacy signals in an ongoing Phase 1/2a clinical trial. The Fore Bio research and development team is optimizing drug development by identifying existing compounds with known clinical profiles and a clear path through clinical development to advance new medicines for patients without treatment options. For more information, please visit or follow us on X (formerly Twitter) and LinkedIn.

Clinical ResultAACRPhase 2Phase 1

13 Mar 2024

·www.biospace.com

C-Suite Shuffle: Sumitomo, Kineta, IDRx and More

Pictured: A red illustration of a businessman walking through a door/iStock, lerbank Welcome to the second in a regular series of rundowns of people coming and going from executive positions at biopharma companies that BioSpace covers. This column will highlight the hired, fired, retired, promoted or resigning, as well as those personally named in lawsuits. While there were no blockbuster moves in the last two weeks on the scale of the Feb. 21 announcement that CEO Richard Gonzalez will soon retire from AbbVie, some less prominent biopharmas shook up their C-suites and others looked toward the next step of growth. Notably, Sumitomo named a new executive officer as part of a restructuring that will include the closure of its CNS sales department, and Kineta halted the enrollment of a clinical trial and cut most of its small staff as it ponders a sale or even liquidation. Meanwhile, IDRx, a member of BioSpace’s 2023 NexGen class, snapped up two execs from Theseus Pharmaceuticals. Alcanza Clinical Research Research facilities network Alcanza Clinical Research has named James Clark its first-ever chief medical officer. Clinical trials specialist Clark was owner and CEO of Charlottesville Medical Research, a Virginia facility that he sold to Alcanza in 2022. Capsida Biotherapeutics Capsida Biotherapeutics has promoted Rob Murphy to chief manufacturing and quality officer from vice president of technical operations. In this role, Murphy will oversee the gene therapy company’s cGMP manufacturing, process development and analytics as Capsida ramps up production of engineered adeno-associated virus–based treatments. Cellipont Bioservices CDMO Cellipont Bioservices has hired Edwin Beale as chief commercial officer. The firm opened a 76,000-square-foot cell therapy manufacturing plant in The Woodlands, Texas, last week. The facility will house a center of excellence in cryopreservation as part of a collaboration with Evia Bio. IDRx IDRx has hired two former Theseus Pharmaceuticals executives to lead the company. Tim Clackson takes over as CEO and Brad Dahms is the new CFO and chief business officer at the Plymouth, Mass.–based clinical-stage targeted cancer therapy startup, which placed 8th in BioSpace’s 2023 NexGen class. Cofounder Ben Auspitz, who relinquished the top role, has been named IDRx chairman. Moligo Technologies Moligo Technologies has named John Kuijpers chief business officer to lead commercialization of the firm’s long, single-stranded DNA for industrial use. The Swedish company has a collaboration with Nationwide Children’s Hospital in Columbus, Ohio, to support research into gene therapies for cystic fibrosis and related conditions. NeoVac NeoVac, a London-based developer of RNA-lipid nanoparticle vaccines and treatments, has hired Heinrich Haas as CTO. Haas previously was VP of RNA formulation and drug delivery at BioNTech. Sumitomo Pharma As part of a restructuring that will result in the loss of 400 jobs in North America and the dissolution of its CNS sales department, Sumitomo Pharma said that Yutaka Wakemi, current vice president in charge of global corporate strategy, will take over as executive officer on April 1. Three executives, Takuya Taguchi, Myrtle Potter and Armin Szegedi, are scheduled to depart March 31. Sumitomo recently reported disappointing sales of three of its drugs. Velsera Velsera has brought in Jamie Littlejohns as CEO to succeed interim leader Hans Cobben, who has returned to his role as board chairman. Littlejohns joined the computational biology company from McKinsey, where he led the consulting firm’s European healthcare and life science private equity practice. He has served as an external adviser to Velsera since 2022, when the company was formed from the merger of Pierian Dx, Seven Bridges and UgenTec. Anagenex Anagenex, an artificial intelligence–driven data generation company supporting small molecule drug discovery, has named Adrian Schreyer chief technology officer. The firm has a nascent research collaboration with Nimbus Therapeutics. Schreyer is former CTO and a founding employee of Exscientia. OncoNano Medicine OncoNano Medicine has promoted Kartik Krishnan to CEO from president and head of R&D, succeeding Martin Driscoll. The Southlake, Texas–based immune-oncology company also promoted Melissa Paoloni to executive VP and chief operating officer. OncoNano has a Phase I trial underway of its ONM-501 dual-activating polyvalent STING agonist for patients with advanced solid tumors and lymphomas. Fore Biotherapeutics Fore Biotherapeutics has brought in William Hinshaw to serve as CEO and board director. Hinshaw, former president, CEO and board member of Axcella Therapeutics, previously headed the U.S. oncology business of Novartis. Fore’s pipeline includes lead asset plixorafenib, a small molecule selective inhibitor of mutated BRAF that is currently in a Phase I/IIa clinical trial in patients with solid tumors. Ionis Pharmaceuticals Ionis Pharmaceuticals has rehired Kyle Jenne to serve as executive VP and chief global strategy officer as the Carlsbad, Calif.–based company prepares to launch its first commercial products. Jenne is replacing Onaiza Cadoret-Manier as head of global project strategy; Cadoret-Manier will depart March 15 but serve as an advisor to Ionis for an unspecified time period. The firm in December received FDA approval for Wainua (eplontersen), a therapy it codeveloped with AstraZeneca for treatment of adult polyneuropathy of hereditary transthyretin-mediated amyloidosis. Alvotech Biosimilars developer Alvotech announced the departure of Chief Quality Officer Sandra Casaca. She has been replaced on an interim basis by Christina Siniscalchi, who recently held a similar title at Alvogen. Days earlier, Alvotech and partner Teva Pharmaceuticals received FDA approval for Simlandi (adalimumab-ryvk), a biosimilar of AbbVie’s Humira (adalimumab). Kineta Kineta announced that it would eliminate the positions of CEO Shawn Iadonato and General Counsel Pauline Kenny as part of a reduction of seven jobs, or 64% of the company’s workforce. Iadonato and Kenny will stay on through the end of the year as Kineta considers a sale, acquisition, liquidation or other alternative. The firm has also stopped enrolling patients in its VISTA-101 Phase I/II trial for its KVA12123 compound for advanced solid tumors. Corbus Pharmaceuticals Corbus Pharmaceuticals has named Dominic Smethurst CMO to lead clinical development of a portfolio of investigational cancer drugs, including CRB-701, a Nectin-4 antibody-drug conjugate. The firm recently closed a $94.5 million public stock offering. Bexion Pharmaceuticals Bexion Pharmaceuticals has appointed a new CMO, Tariq Arshad, an oncologist who previously led R&D at Qualigen Therapeutics. Bexion is developing biologics to treat solid tumors and chemotherapy-induced peripheral neuropathy. Nicox Nicox fired CEO Andreas Segerros and replaced him with Gavin Spencer on the same day that the French ophthalmology drug company announced a restructuring of its debt to extend its cash runway to November 2024. The firm is concentrating its efforts on landing new financing to complete a Phase III trial of its lead asset, an investigational glaucoma therapy called NCX 470, by generating enough data to New Drug Application with the FDA. Nicox recently inked a partnership with Kowa to develop and commercialize the drug in Japan. Neil Versel is the business editor at BioSpace. You can reach him at neil.versel@biospace.com. Follow him on LinkedIn or X.

Executive ChangePhase 1Drug Approval

29 Feb 2024

·www.biospace.com

FORE Biotherapeutics Names William R. Hinshaw as Chief Executive Officer

PHILADELPHIA--(BUSINESS WIRE)-- FORE Biotherapeutics today announced the appointment of William R. Hinshaw as the Chief Executive Officer and Director of the Board. Mr. Hinshaw is a 30+-year veteran of the biotechnology and pharmaceutical industries. Prior to joining Fore, he was the President, CEO and Board member of Axcella Therapeutics, a clinical-stage and publicly traded biopharmaceutical company developing novel therapies for complex diseases. Prior to Axcella, Mr. Hinshaw led all aspects of Novartis’ >$6B revenue U.S. Oncology business, including products such as Tasigna®, Gleevec®, and Kymriah®, as well as the integration of the GSK oncology portfolio, including Tafinlar® and Mekinist®. He also played a key role on the Global Oncology Executive Committee, including leading crucial strategic programs to maximize the portfolio and develop the pipeline. Prior to this role, Mr. Hinshaw held a number of leadership positions of increasing responsibility and expanding global scope at Novartis, including Head of the NCE (Northern and Central Europe) Region for Novartis Oncology, GEM (Group Emerging Markets), Head of the Hematology Business Franchise, and Global Head of Infectious Disease and Transplantation (IDTI). Before joining Novartis, Bill worked at the former Schering Plough Corporation where he held a series of commercial roles, including the Head of US Oncology. Mr. Hinshaw holds a B.S. in Molecular Biology from the University of Wisconsin. Dieter Weinand, the Chairman of the Board of Directors commented: “After an extensive search, we are delighted and very excited to welcome Bill as our next CEO. Bill brings highly relevant experience to grow and scale Fore given his track record in both large and emerging life sciences companies. He is the right leader for this stage of our company’s journey and the Board and I are delighted to partner with Bill to navigate Fore’s path to continued success.” “I am privileged and excited to lead Fore and work alongside the talented and committed team and build upon what has been accomplished to date. Fore is poised to develop targeted treatments that can have a transformational impact on the lives of patients suffering from cancer,” said Mr. Hinshaw. “On behalf of the Board of Directors, I would like to sincerely thank Dr. Shawn M. Leland, PharmD, RPh for his leadership, dedication and many contributions during this transitionary period toward the advancement of plixorafenib to its next seminal phase of clinical development as Advisor and Interim CEO to the Company,” said Dieter Weinand, Chairman of the Board of FORE Biotherapeutics. “We welcome Bill as CEO and Board member as we enter this next phase of growth for the company.” About Plixorafenib Plixorafenib is an investigational, novel, small-molecule, next-generation, orally available selective inhibitor of mutated BRAF. It was designed to target a wide range of BRAF mutations while sparing wild-type forms of RAF. Preclinical studies and clinical trials have shown that its unique mechanism of action effectively inhibits not only the constitutively active BRAFV600 monomers targeted by first-generation RAF inhibitors but also disrupts constitutively active dimeric BRAF class 2 mutants, fusions, splice variants and others. Unlike first-generation RAF inhibitors, plixorafenib does not induce paradoxical activation of the RAF/MEK/ERK pathway. As a “paradox breaker”, plixorafenib could therefore treat acquired resistance to current RAF inhibitors and, more generally, yield improved safety and more durable efficacy than first-generation RAF inhibitors. Plixorafenib is currently being evaluated in Phase 1/2a clinical trial in patients with advanced solid tumors (including brain and spinal cord tumors) with activating BRAF alterations. Interim clinical data presented at ESMO 2022, ASCO 2023 and SNO 2023 provided evidence of durable anti-tumor activity in patients with BRAF-mutated cancers. About FORE Biotherapeutics Fore Bio is a precision oncology company dedicated to developing innovative treatments that provide better outcomes for patients with the hardest-to-treat cancers. The Company’s lead asset plixorafenib (FORE8394; formerly PLX8394) is an inhibitor of BRAF dimerization allowing for the targeting of V600 and non-V600 driven tumors. In Phase 1/2a, plixorafenib demonstrated deep and durable responses in V600-mutated MAPK inhibitor-naïve patients, including a 42% overall response in patients with solid tumors with a median duration of response of 17.8 months and a 67% overall response rate in patients with primary central nervous system tumors with a median duration of response of 13.9 months. Plixorafenib is currently being investigated in the ongoing, potentially registrational Phase 2 FORTE study. For more information, please visit or follow us on X (formerly Twitter) and LinkedIn.

Executive ChangePhase 2Clinical ResultPhase 1

100 Deals associated with Plixorafenib

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R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
BRAF mutation Solid Tumors	Phase 2	US	Fore Biotherapeutics, Inc.	21 Feb 2023
BRAF mutation Solid Tumors	Phase 2	CA	Fore Biotherapeutics, Inc.	21 Feb 2023
BRAF mutation Solid Tumors	Phase 2	FR	Fore Biotherapeutics, Inc.	21 Feb 2023
BRAF mutation Solid Tumors	Phase 2	DE	Fore Biotherapeutics, Inc.	21 Feb 2023
BRAF mutation Solid Tumors	Phase 2	IT	Fore Biotherapeutics, Inc.	21 Feb 2023
BRAF mutation Solid Tumors	Phase 2	KR	Fore Biotherapeutics, Inc.	21 Feb 2023
BRAF mutation Solid Tumors	Phase 2	ES	Fore Biotherapeutics, Inc.	21 Feb 2023
BRAF mutation Solid Tumors	Phase 2	SE	Fore Biotherapeutics, Inc.	21 Feb 2023
BRAF mutation Solid Tumors	Phase 2	GB	Fore Biotherapeutics, Inc.	21 Feb 2023
Advanced Malignant Solid Neoplasm	Phase 2	US	Fore Biotherapeutics, Inc.	01 Apr 2015

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT02428712 (ASCO2023) Manual	Phase 2	BRAF-mutation brain cancer \| HR-positive/HER2-low Solid Tumors BRAF	110	Plixorafenib±cobicistat	guieygpvzn(jjwxkycgku) = Dose-limiting toxicities were only observed at doses ≥1500 mg/day + cobi: 1500-1800 mg/day (4) and 2700-3600 mg/day (1). esenzqytvz (hdfqbidunm )	Positive	31 May 2023
NCT02428712 (ASCO2023) Manual	Phase 1/2	HR-positive/HER2-low Solid Tumors \| Central Nervous System Neoplasms	110	FORE8394	rhbmivoeiq(dacqecmfjx) = cclfmgzdsd epuxawruxj (zybestvfze ) View more	Positive	26 May 2023
NCT02428712 (ASCO2023) Manual	Phase 1/2		110	FORE8394 (pts with MAPKi-naïve, V600 mutant tumors (excluding colorectal cancer [CRC]))	apkoqdyfjc(mzmnejtrva) = pkcdmayagg nsoqcgklwe (wwhmpskxuh )	Positive	26 May 2023
NCT02428712 (ESMO2020)	Phase 1/2	Advanced cancer	69	PLX8394	oygjxbklix(tzlrcjbvtw) = 4 pts mafzdpfppq (hpvoxaqdbo ) View more	Positive	18 Sep 2020
NCT02428712 (ASCO2018) Manual	Phase 1/2	BRAF mutation Solid Tumors BRAF Mutation	31	PLX8394+cobicistat	uzaegrmome(xqahtgvxdw) = fcrrporrmg okgakndwar (kgtfcsfnlv )	Positive	04 Jun 2018
NCT02428712 (ASCO2018) Manual	Phase 1/2	BRAF mutation Solid Tumors BRAF Mutation	31	PLX8394+cobicistat	obsjomjbby(sbgbhrgofw) = inezwsoqnv ikwmtxwjkq (ltcnitnrtz ) View more	Positive	04 Jun 2018

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