MEK1 inhibitors(Dual specificity mitogen-activated protein kinase kinase 1 inhibitors), MEK2 inhibitors(Dual specificity mitogen-activated protein kinase kinase 2 inhibitors)

Therapeutic Areas

NeoplasmsEndocrinology and Metabolic DiseaseRespiratory Diseases+ [7]

Active Indication

BRAF mutated anaplastic thyroid cancerThyroid Cancer with BRAF mutationBRAF V600E mutant Non-small Cell Lung Cancer+ [29]

Inactive Indication

Acute Myeloid LeukemiaAdenocarcinoma of LungAdvanced Bile Duct Carcinoma+ [34]

Originator Organization

Array BioPharma, Inc.

Active Organization

Pfizer Inc.Pierre Fabre Médicament SASPierre Fabre Medicament Information

+ [10]

Inactive Organization

Novartis Pharmaceuticals Corp.

Deciphera Pharmaceuticals, Inc.

Plexxikon, Inc.

Drug Highest PhaseApproved

First Approval Date

US (27 Jun 2018),

BRAF V600 mutation-positive Melanoma

RegulationOrphan Drug (US)

Structure/Sequence

Molecular FormulaC17H15BrF2N4O3

InChIKeyACWZRVQXLIRSDF-UHFFFAOYSA-N

CAS Registry606143-89-9

149

Clinical Trials associated with Binimetinib

NCT05554354

/ Active, not recruitingPhase 2IIT

Phase 2 Trial of Fulvestrant and Binimetinib in Patients With Hormone Receptor-Positive Metastatic Breast Cancer With Inactivating or Inferred Inactivating NF1 Alterations: A ComboMATCH Treatment Trial

This phase II ComboMATCH treatment trial compares the usual treatment alone (fulvestrant) to using binimetinib plus the usual treatment in patients with hormone receptor positive breast cancer that has spread from where it first started to other places in the body (metastatic) and has an NF1 genetic change. Fulvestrant is a hormonal therapy that binds to estrogen receptors in tumor cells, resulting in estrogen receptor destruction and decreased estrogen binding, which may inhibit the growth of estrogen-sensitive tumor cells. Binimetinib is a targeted therapy that may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. The addition of binimetinib to fulvestrant in breast cancers with an NF1 genetic change could increase the percentage of tumors that shrink as well as lengthen the time that the tumors remain stable (without progression) as compared to fulvestrant alone.

Start Date13 Sep 2024

Sponsor / Collaborator

National Cancer Institute

[+1]

NCT05615818

/ RecruitingPhase 3IIT

Molecular Targeted Maintenance Therapy Versus Standard of Care in Advanced Biliary Cancer: an International, Randomised, Controlled, Open-label, Platform Phase 3 Trial

The object of this trial is to evaluate whether the introduction of a targeted therapy after 4 cycles of the current standard-of-care treatment for advanced biliary cancer is superior to continuing with the standard treatment.
The trial is composed of two phases: (i) An initial screening phase to identify a suitable patient population, during which a molecular profile of the patient's tumour will be obtained, and (ii) a randomised comparative trial in which patients with disease control after 4 cycles of standard treatment, and whose tumour harbours a targetable molecular alteration, will be randomised (2:1) to receive either a matched targeted therapy or to continue with the standard treatment.

Start Date18 Jul 2024

Sponsor / Collaborator

UNICANCER

[+8]

NCT06207656

/ RecruitingPhase 2IIT

Multicenter Phase 2 Study to Evaluate the Efficacy and Safety of Cetuximab in Combination with Encorafenib Plus Binimetinib As Induction Treatment in BRAF V600E Mutated MSS Initially Resectable or Potentially Resectable Advanced Colorectal Cancer

As a result of the little benefit obtained from standard treatments and the poor prognosis of these patients, the BRAF-V600E mutant MSS aCRC represents an unmet medical need requiring clinical research.
The combination of encorafenib, cetuximab and binimetinib as second- or third-line treatment for mCRC resulted in significantly better outcomes than standard therapy in a phase 3 clinical trial, which also revealed treatment safety and tolerability to be acceptable. Compared to the control group (cetuximab and irinotecan or cetuximab and FOLFIRI), the triplet therapy cohort showed higher median overall survival (9.3 vs. 5.9 months) and response rates (26.8% vs. 1.8%). Grade 3 adverse events occurred in 65.8% and 64.2% of patients for triple-therapy and control groups, respectively.
Based on these results, the investigators speculated that the combination of encorafenib, cetuximab and binimetinib could be used as induction therapy to improve treatment outcomes in BRAF-V600E-mutated MSS aCRC locally advanced initially unresectable but potentially resectable; initially resectable or initially unresectable but potentially resectable oligometastatic disease; and in patients with stage II-IV who have relapsed after chemotherapy (neo and/or adjuvant) or surgery, if the shorter time after resection or from treatment end to relapse is longer than 6 months.

Start Date16 Apr 2024

Sponsor / Collaborator

Merck & Co., Inc.

100 Clinical Results associated with Binimetinib

100 Translational Medicine associated with Binimetinib

100 Patents (Medical) associated with Binimetinib

692

Literatures (Medical) associated with Binimetinib

01 May 2025·INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES

Effects of F53 hotspot mutations on the molecular dynamics of MEK1 protein and the binding of its FDA-approved inhibitors

Article

Author: Vural, Berkin Ersin ; Yandım, Cihangir

MEK1 (MAP2K1) could emerge as an oncogenic protein in the presence of certain mutations, and could be inhibited by FDA-approved drugs (trametinib, cobimetinib, binimetinib and selumetinib). However, how the mutations on MEK1's hotspot residue F53 affect the bindings of these therapeutic molecules remained largely unexplored. We performed molecular dynamics (MD) simulations with wild-type and mutated (F53L/V/C/I/Y) MEK1 structures in the presence and absence of these drugs and observed changes on the motion of MEK1. A longer duration in the lowest energy state conformation was observed during the simulations in the presence of F53 mutations. This was complemented by cross-correlated motions of amino acids of MEK1. More importantly, the binding affinities of inhibitors were affected. There was a marked reduction in the calculated binding affinity of trametinib in the presence of F53C mutation. On the other hand, the binding affinities of cobimetinib and selumetinib could overcome F53 mutations on MEK1. Binimetinib interestingly exhibited an increased binding affinity when F53C/I mutations were present. Taken together, our results provide a comprehensive perspective on the structural and drug-binding effects of observed mutations on the hotspot residue F53 within MEK1; warranting further research in stratifying F53 hotspot mutations for effective drug binding.

01 Apr 2025·MELANOMA RESEARCH

Neurologic adverse events associated with BRAF and MEK inhibitor therapy in patients with malignant melanoma: a disproportionality analysis using the Food and Drug Administration Adverse Event Reporting System

Article

Author: Jedlowski, Patrick ; Leibovit-Reiben, Zachary ; Thiede, Rebecca ; Godfrey, Hannah

BRAF and MEK inhibitor (BRAFi + MEKi) therapy has improved the treatment of solid tumors with BRAF mutation. However, their neurologic adverse events (nAEs) have been largely unexplored. This study aimed to provide clinicians with more updated knowledge on nAEs associated with BRAFi + MEKi therapy in patients with malignant melanoma compared with nonmelanoma cancers. The United States Food and Drug Administration Adverse Event Reporting System was queried from 2011 to 2022 to capture nAEs reported for the BRAFi + MEKi therapies, vemurafenib plus cobimetinib (V + C), dabrafenib plus trametinib (D + T), and encorafenib plus binimetinib (E + B). A disproportionality analysis was performed to calculate their reporting odds ratios (RORs) and 95% confidence intervals (CIs) using a control group of antineoplastic medications. There were 2881 BRAFi + MEKi therapy-associated nAE cases, the majority of which listed malignant melanoma as the reason for use (87.5, 66.7, and 62.0% for V + C, D + T, and E + B, respectively). Several novel associations were identified; including epidural lipomatosis (ROR: 320.07, 95% CI: 123.76–827.77 for V + C), peripheral nerve lesion (ROR: 185.64, 95% CI: 73.95–466.03 for V + C), Guillain-Barre syndrome (RORs: 8.80, 2.94, and 11.79, 95% CIs: 3.65–21.22, 1.40–6.19, and 5.87–23.66 for V + C, D + T, and E + B), demyelinating polyneuropathy (RORs: 24.72 and 78.98, 95% CI: 8.16–74.86 and 24.84–251.13 for D + T and E + B), and multiple sclerosis (ROR: 5.90, 95% CI: 3.06–11.40 for D + T) in melanoma patients. nAEs in the setting of BRAFi + MEKi therapy should be a safety consideration when utilizing these medications.

03 Mar 2025·CLINICAL CANCER RESEARCH

Triple Combination of MEK, BET, and CDK Inhibitors Significantly Reduces Human Malignant Peripheral Nerve Sheath Tumors in Mouse Models

Article

Author: Ferrer, Marc ; Diazgranados, Adriana Paola ; Mazuelas, Helena ; Gel, Bernat ; Blanco, Ignacio ; Ortega-Bertran, Sara ; Serra, Eduard ; Salvador, Héctor ; Magallón-Lorenz, Miriam ; Lázaro, Conxi ; Zhang, Xiaohu ; Romagosa, Cleofé ; De Raedt, Thomas ; Valverde, Claudia ; Creus-Bachiller, Edgar ; Uriarte-Arrazola, Itziar ; Villanueva, Alberto ; Fernández-Rodríguez, Juana ; Carrió, Meritxell

Abstract:

Purpose::

Malignant peripheral nerve sheath tumor (MPNST) is an aggressive soft-tissue sarcoma that develops sporadically or in patients with neurofibromatosis type 1 (NF1). Its development is marked by the inactivation of specific tumor suppressor genes (TSG): NF1, CDKN2A, and SUZ12/EED (polycomb repressor complex 2). Each TSG loss can be targeted by particular drug inhibitors, and we aimed to systematically combine these inhibitors, guided by TSG inactivation status, to test their precision medicine potential for MPNSTs.

Experimental Design::

We performed a high-throughput screening in 3 MPNST cell lines testing 14 MEK inhibitors (MEKi), 11 cyclin-dependent kinase 4/6 inhibitors (CDKi), and 3 bromodomain inhibitors (BETi) as single agents and 147 pairwise co-treatments. Best combinations were validated in nine MPNST cell lines, and three were tested in one sporadic and one NF1-associated patient-derived orthotopic xenograft (PDOX) MPNST mouse model. A final combination of the three inhibitor classes was tested in the same PDOX models.

Results::

A high degree of redundancy was observed in the effect of compounds of the same inhibitory class, individually or in combination, and responses matched with TSG inactivation status. The MEKi–BETi (ARRY-162 + I-BET151) co-treatment triggered a reduction in half of the NF1-related MPNST PDOXs and all the sporadic tumors, reaching 65% reduction in tumor volume in the latter. Remarkably, this reduction was further increased in both models combining the three inhibitor classes, reaching 85% shrinkage on average in the sporadic MPNST.

Conclusions::

Our results strongly support precision therapies for MPNSTs guided by TSG inactivation status. MEKi–BETi CDKi triple treatment elicits a significant reduction of human MPNST PDOXs.

News (Medical) associated with Binimetinib

03 Feb 2025

·www.biopharmadive.com

Pfizer drug acquired in $11B buyout confirms benefit in colon cancer

Dive Brief:Adding Pfizers cancer drug Braftovi to standard treatments helped people with a form of colorectal cancer live longer without their disease worsening than those who got the typical care alone in a Phase 3 trial, the company said Monday.The result confirms earlier research from the study, called Breakwater, which had shown that trial volunteers receiving Braftovi were significantly more likely to see their tumors shrink or disappear. Those data were used to support an accelerated U.S. clearance for Braftovi in colorectal cancer in December.Pfizer has been under pressure from investors to grow revenue amid plummeting sales for its COVID-19 treatments, and cancer drug research is one area it hopes can pick up the slack. Braftovi and the related drug Mektovi, which Pfizer acquired in a 2019 deal for Array BioPharma, generated $437 million in sales through the first nine months of 2024.Pfizer reports full-year earnings on Tuesday.Dive Insight:Braftovi is a targeted medicine aimed at a particular mutation, V600E, to the BRAF gene.BRAF mutations occur in about 10% of people with colorectal cancer, and the V600E is the most common among them.A regimen of Braftovi and Mektovi is already approved in skin and lung cancers. In colorectal tumors, the drug is used in advanced disease with a drug called cetuximab. Those two are prescribed alongside chemotherapy in the frontline setting under the speedy clearance issued in December.Pfizer acquired Braftovi and Mektovi in an $11.4 billion buyout of Array BioPharma in 2019. At the time, the two drugs were only cleared for melanoma. Pfizer broadened use to other tumors afterward, but they still only generate modest revenue compared to other cancer drugs in the companys portfolio. The new results revealed on Monday could boost those numbers, though, as Pfizer claimed, without revealing specific details, that Braftovi helped delay tumor progression and extend the lives of colorectal cancer patients.Since the Array deal, Pfizer has shifted away from targeted small-molecule drugs for cancer and towards biologics. Antibody-drug conjugates, such as those acquired in a $43 billion deal for Seagen, are a focus and part of a plan to have biologics account for 65% of its oncology revenue by 2030 compared to only 6% in 2023.Patents for two of Pfizers biggest sellers in cancer, Xtandi and Ibrance, expire in 2027. '

AcquisitionPhase 3Drug ApprovalClinical ResultADC

09 Jan 2025

·www.businesswire.com

FORE Biotherapeutics Highlights Recent Pipeline Achievements for its Targeted-Oncology Program and Provides Strategic Objectives for 2025

PHILADELPHIA--( BUSINESS WIRE )--FORE Biotherapeutics, a registration stage biotherapeutics company dedicated to developing targeted therapies to treat patients with cancer, today highlighted its recent pipeline achievements and provided its key strategic objectives for 2025. William Hinshaw, Chief Executive Officer of Fore Biotherapeutics, will detail progress and discuss anticipated milestones in a presentation at the 43 rd Annual J.P. Morgan Healthcare Conference. The presentation will take place on Tuesday, January 14, 2025, at 5:30 p.m. PT in San Francisco, CA. “ 2025 will be an exciting year at Fore, with multiple value-creating catalysts anticipated in the near-term across our trials. Our focus in 2025 will be continued execution of our differentiated monotherapy development of plixorafenib, which represents a multi-billion dollar opportunity, and the potential for expansion into developing plixorafenib as a combination agent. Plixorafenib’s unique mechanism of action supports the potential to reset the standard for patients with BRAF driven tumors, which have been underserved and underpenetrated due to the limitations of current agents. Plixorafenib is designed to inhibit not only the constitutively active BRAFV600 monomers targeted by first-generation RAF inhibitors, but also disrupt constitutively active dimeric BRAF class II mutants, fusions, splice variants and others, which differentiates it from current approved therapies. We are encouraged by the compelling safety and efficacy profile we have seen and the progress in our registrational trials,” said William Hinshaw, Chief Executive Officer of Fore. 2024 Achievements Strengthened Leadership Team: In 2024, Fore strengthened its leadership team with the appointment of William Hinshaw as Chief Executive Officer, Michael Byrnes as Chief Financial Officer and Payman Darouian, as Senior Vice President, Corporate Development, Strategy and Commercial. The new management team brings extensive experience from large pharmaceutical companies and multiple high-growth, publicly traded biotechnology companies adding to the strong existing capabilities of the team. Continued Execution of FORTE Master Protocol: The FORTE Master Protocol is a global clinical trial which includes baskets evaluating plixorafenib in distinct patient populations. The three monotherapy indications currently under evaluation are BRAF V600 Recurrent Primary Central Nervous System (CNS) Tumors, Rare BRAF V600 Mutated Solid Tumors and Solid Tumors with BRAF Fusions. Advanced Plixorafenib in BRAF V600 Recurrent Primary Central Nervous System Tumors: Continued enrollment in registration-intended basket in up to 50 patients with BRAF V600-mutated recurrent primary CNS tumors. This BOP2 design trial enrolls patients who are naïve to MAPK pathway inhibitor (MAPKi) treatment. Major efficacy endpoints include overall response rate (ORR) and duration of response (DOR). The study builds upon a previous clinical trial of plixorafenib in which six out of nine, or 67%, of MAPKi naïve adults with recurrent BRAF V600-mutated primary CNS tumors demonstrated a partial response (PR) with a median DOR (mDOR) of 13.9 months. Advanced Plixorafenib in Rare BRAF V600 Mutated Solid Tumors: Initiated enrollment in registration-intended basket in up to 75 patients with rare BRAF V600-mutated solid tumors. This BOP2 design trial enrolls patients who are naïve to MAPKi treatment. Major efficacy endpoints include ORR and DOR. The study builds upon a previous clinical trial of plixorafenib in which 42% of MAPKi naïve adults with BRAF V600-mutated solid tumors demonstrated a PR with a mDOR of 17.8 months. Advanced Plixorafenib in Solid Tumors with BRAF Fusions: Continued enrollment in registration-intended basket in up to 75 patients with BRAF fusion advanced solid tumors. This BOP2 design trial enrolls patients with tumors harboring BRAF fusions, excluding those with prior treatment with MAPK inhibitors as well as patients with colorectal or pancreatic ductal adenocarcinoma. The primary endpoint is ORR, as determined by RANO criteria or RECIST v1.1 for primary CNS tumors or other solid tumors, respectively. The study builds upon a previous clinical trial of plixorafenib that demonstrated promising single agent activity including one complete response with a DOR of 66.7+ months, one PR with a DOR of 9.2+ months, and seven stable disease, out of 14 adults evaluable for efficacy. Reported Supportive Nonclinical Data at AACR 2024: Fore reported nonclinical data at AACR 2024 demonstrating that plixorafenib in combination with binimetinib, a MEK inhibitor, is more potent than other BRAF and pan-RAF inhibitors combined with binimetinib, as well as the synergistic activity of plixorafenib with MEK inhibition across all BRAF alterations tested. Reported Supportive Safety and Efficacy Data at International Symposium on Pediatric Neuro-Oncology (ISPNO 2024): Fore reported safety and efficacy data at ISPNO 2024 building on the existing evidence of plixorafenib in children and adults with BRAF-altered recurrent primary CNS tumors. Reported Supportive Safety and Efficacy Data in Ovarian Cancer at 15 th Biennial Ovarian Cancer Research Symposium (OCRS): Fore reported safety and efficacy data at OCRS 2024, including durable partial responses in three out of three patients with BRAF V600-mutated ovarian cancer, who were all heavily pre-treated. 2025 Strategic Objectives and Anticipated Milestones Continued Execution of the FORTE Master Protocol with Interim Analyses in Three Monotherapy Indications Anticipated in 2025 BRAF V600 Primary Recurrent Central Nervous System Tumors: An interim efficacy analysis from the first 25 evaluable patients is anticipated to be conducted in the third quarter of 2025. Pending a positive recommendation from the data monitoring committee, topline data from this trial would be anticipated in the second half of 2026. The company anticipates that this trial, with sufficient demonstration of safety and efficacy, would enable the submission of a New Drug Application (NDA) to the U.S. Food and Drug Administration (FDA) under the Accelerated Approval pathway. Rare BRAF V600 Mutated Solid Tumors: An interim efficacy analysis from the first 25 evaluable patients is anticipated to be conducted in the fourth quarter of 2025. Advanced Solid Tumors with BRAF Fusions: An interim efficacy analysis from the first 25 evaluable patients is anticipated to be conducted in the fourth quarter of 2025. About FORE Biotherapeutics Fore is a registration stage targeted 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 rationally designed with a first-in-class mechanism to address treatment gaps from 1 st and 2 nd generation BRAF inhibitors. Plixorafenib has demonstrated single-agent efficacy signals across a variety of tumor types with a manageable safety profile in a Phase 1/2a clinical trial of over 100 patients and is currently enrolling patients in FORTE, a global registrational basket trial to support three distinct indications. For more information, please visit www.fore.bio or follow us on X and LinkedIn .

Clinical ResultExecutive Change

07 Jan 2025

·endpts.com

Immuneering touts positive pancreatic cancer data for MEK inhibitor

Immuneering’s shares rocketed in premarket trading on Tuesday on the back of positive mid-stage data for its MEK inhibitor in pancreatic cancer, sparking plans to add more combination arms. Three out of seven patients with first-line pancreatic cancer given the biotech’s IMM-1-104 plus modified gemcitabine/nab-paclitaxel reached a complete or partial response in the Phase 2a study, according to a release . The numbers translate to a 43% overall response rate. For context, gemcitabine/nab-paclitaxel are linked to a 23% ORR in this setting, according to the company. Immuneering’s shares $IMRX were up 44% at market open Tuesday, though the stock was trading up at about 5% by mid-morning. Several MEK inhibitors are already on the market for melanoma including Pfizer’s Mektovi and Novartis’ Mekinist. But these treatments are mainly approved to treat patients with BRAF-driven tumors. Immuneering said IMM-1-104 is designed to be effective in a broader range of cancers — including RAS-mutated tumors — and could offer better safety. In a separate cohort of Phase 2 patients with first-line pancreatic cancer, all four evaluable subjects treated with IMM-1-104 plus modified FOLFIRINOX saw tumor shrinkage and disease control. Elsewhere, eleven out of 21 second-line pancreatic cancer patients given IMM-1-104 as a single agent achieved disease control. The company said the drug was “very well tolerated” in this cohort, with all side effects grade 1 or 2 in severity. Following the positive results, Immuneering plans to add more cohorts to the trial — one will test IMM-1-104 with a BRAF inhibitor in certain patients with melanoma, and two others will evaluate the drug plus checkpoint inhibitors in melanoma and non-small cell lung cancer. Back in September, the drugmaker reported initial promising results from five pancreatic cancer patients. At the time, Chardan analysts cautioned the data “came from a very small number of patients.”

Clinical ResultPhase 2Phase 1

100 Deals associated with Binimetinib

External Link

KEGG	Wiki	ATC	Drug Bank
D10604	Binimetinib	L01XE41	DB11967

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
BRAF mutated anaplastic thyroid cancer	JP	Ono Pharmaceutical Co., Ltd.	17 May 2024
Thyroid Cancer with BRAF mutation	JP	Ono Pharmaceutical Co., Ltd.	17 May 2024
BRAF V600E mutant Non-small Cell Lung Cancer	US	Array BioPharma, Inc.	11 Oct 2023
BRAF Mutation colorectal cancers	JP	Ono Pharmaceutical Co., Ltd.	27 Nov 2020
BRAF mutation positive Melanoma	JP	Ono Pharmaceutical Co., Ltd.	08 Jan 2019
Melanoma	AU	Pierre Fabre SA	03 Jan 2019
BRAF V600 mutation-positive Melanoma	US	Array BioPharma, Inc.	27 Jun 2018

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Melanoma, Cutaneous Malignant	Phase 3	AR	Pierre Fabre Médicament SAS	02 May 2022
Melanoma, Cutaneous Malignant	Phase 3	AU	Pierre Fabre Médicament SAS	02 May 2022
Melanoma, Cutaneous Malignant	Phase 3	AT	Pierre Fabre Médicament SAS	02 May 2022
Melanoma, Cutaneous Malignant	Phase 3	BE	Pierre Fabre Médicament SAS	02 May 2022
Melanoma, Cutaneous Malignant	Phase 3	BR	Pierre Fabre Médicament SAS	02 May 2022
Melanoma, Cutaneous Malignant	Phase 3	CA	Pierre Fabre Médicament SAS	02 May 2022
Melanoma, Cutaneous Malignant	Phase 3	CZ	Pierre Fabre Médicament SAS	02 May 2022
Melanoma, Cutaneous Malignant	Phase 3	FR	Pierre Fabre Médicament SAS	02 May 2022
Melanoma, Cutaneous Malignant	Phase 3	DE	Pierre Fabre Médicament SAS	02 May 2022
Melanoma, Cutaneous Malignant	Phase 3	GR	Pierre Fabre Médicament SAS	02 May 2022

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


JPRN-UMIN000045530 (BEETS trial (JACCRO CC-18), ASCO_GI2025)	Phase 2/3	BRAF Mutation colorectal cancers	203	Encorafenib and cetuximab with binimetinib	bvreafsexn(nkabthsjzh) = lljsbzazzr gztrmyqeik (mckjfiqcwu ) View more	Positive	23 Jan 2025
				Encorafenib and cetuximab without binimetinib	bvreafsexn(nkabthsjzh) = fvnorhbjlx gztrmyqeik (mckjfiqcwu ) View more
NCT03843775 (CTgov)	Phase 1/2	BRAF mutation Solid Tumors	17	Encorafenib+Binimetinib (Dose Level 1)	lyfmdaeilf(micvfsoxlo) = yppyfdvxsd cyenooqvbc (kvykitdelu, adbutdigjl - rhjuepkhtz) View more	-	21 Oct 2024
				Encorafenib+Binimetinib (Dose Level 2)	vkhbjdfbpl(nvprkxxvwo) = weqzpvqyvl jywewgbfkx (tpatvzxhgz, tudqbxqtuq - ybvlyuyuko) View more
NCT03864042 (CTgov)	Phase 1	Advanced Malignant Solid Neoplasm \| Metastatic melanoma \| Unresectable Melanoma ... View more	56	omeprazole+encorafenib+midazolam+caffeine+binimetinib+dextromethorphan+losartan (Arm 1 - CYP Probe Cocktail)	ahxpqkuthe(gqhhooevkx) = poxutqhwzk ibxdclvjbs (zmjcvmpyny, mwdtxemrep - mjqcowkfko) View more	-	27 Sep 2024
				rosuvastatin+bupropion immediate release (IR)+encorafenib+binimetinib (Arm 2 - Rosuvastatin and Bupropion)	wausvrmwrk(yfzvwysiqc) = ytwvyncetg ldruatbfdh (barkgmbsaj, yphxekskyo - eabppuckto) View more
NCT04526782 (IFCT-1904 \| ENCO-BRAF, ESMO2024) Manual	Phase 2	BRAF V600E mutant Non-small Cell Lung Cancer First line BRAF V600E-mutant	64	encorafenib 450mgbinimetinib	atwrhyrwzo(wmifkvgdcm) = twtgktxtqp abwrhghbof (keykujwijg, 55.0 - 78.3) View more	Positive	14 Sep 2024
NCT03915951 (PHAROS, WCLC2024) Manual	Phase 2	BRAF V600E mutant Non-small Cell Lung Cancer Second line \| First line BRAF V600E	98	Encorafenib 450 mBinimetiniby plus Binimetinib 45 mg twice daily	xeesfnbhfz(vpvavflltm) = qnnyfhxafb usqqnklwni (odyjflopqy ) View more	Positive	10 Sep 2024
				EncorafenibBinimetinib	xeesfnbhfz(vpvavflltm) = vbnlvrigls usqqnklwni (odyjflopqy ) View more
ESMO_GI2024 Manual	Not Applicable	BRAF V600E mutant Colorectal Cancer BRAF V600E	489	Encorafenib+Binimetinib+Cetuximab	jynublneqj(aixvwkfvdb) = noponbdtbb syptolttbd (inzocilntv, 0.14 - 0.64) View more	Positive	27 Jun 2024
NCT03235245 (EBIN, ASCO2024) Manual	Phase 2	BRAF V600K Mutation-Positive Melanoma \| BRAF V600E Mutation-Positive Melanoma BRAF V600K \| BRAF V600E	135	Nivolumab + Ipilimumab	plrgzmygyb(frdnjaobwl): HR = 0.87 (90% CI, 0.67 - 1.12), P-Value = 0.36 View more	Negative	02 Jun 2024
				Encorafenib + Binimetinib +ipilimumab +nivolumab
NCT03839342 (BEAVER, ASCO2024) Manual	Phase 2	Advanced Malignant Solid Neoplasm Non-V600 BRAF Mutation	23	Binimetinibencorafenib	yqerzsksnl(zbmpchpziy) = nquhlnpywi nsxvxsuypv (yqozmwdcfc ) View more	Negative	24 May 2024
				Binimetinib + encorafenib (TP53 mts)	yomgbopzhu(chrxjxnnan) = oarkktasfg qyfcsjgmll (qukcdpewzn )
Dutch Melanoma Treatment Registry (ASCO2024)	Not Applicable	Metastatic melanoma First line Lactate dehydrogenase levels	208	Encorafenib/binimetinib	unwspqdvbh(tnoixperlr) = ggigxaocsk stmjndvcch (aniwplljsi ) View more	Positive	24 May 2024

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