Delving into the Latest Updates on Futibatinib with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

Futibatinib (JAN/USAN/INN), TAS 120, TAS-120

+ [2]

Target

FGFR1 x FGFR2 x FGFR3 x FGFR4

Action

antagonists

Mechanism

FGFR1 antagonists(Fibroblast growth factor receptor 1 antagonists), FGFR2 antagonists(Fibroblast growth factor receptor 2 antagonists), FGFR3 antagonists(Fibroblast growth factor receptor 3 antagonists)

Therapeutic Areas

NeoplasmsDigestive System DisordersOther Diseases+ [5]

Active Indication

FGFR2 fusion or rearranged CholangiocarcinomaIntrahepatic CholangiocarcinomaBiliary Tract Neoplasms+ [21]

Inactive Indication

KRAS Mutant Pancreatic CancerNon-Small Cell Lung Cancer

Originator Organization

Taiho Pharmaceutical Co., Ltd.

Active Organization

Taiho Oncology, Inc.

Taiho Pharmaceutical Co., Ltd.Merck Sharp & Dohme LLC

Inactive Organization-

Drug Highest PhaseApproved

First Approval Date

United States (30 Sep 2022),

Intrahepatic Cholangiocarcinoma

RegulationAccelerated Approval (United States), Orphan Drug (United States), Orphan Drug (European Union), Orphan Drug (Australia), Conditional marketing approval (European Union), Priority Review (United States), Breakthrough Therapy (United States)

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Structure/Sequence

Molecular FormulaC22H22N6O3

InChIKeyKEIPNCCJPRMIAX-HNNXBMFYSA-N

CAS Registry1448169-71-8

The FUTURE trial is a prospective, multicentre, exploratory, open-label phase II platform trial. Its goal is to evaluate the efficacy, feasibility and safety of futibatinib combined with immunotherapeutic, targeted or chemotherapeutic agents in colorectal and other solid tumors and to additionally identify biomarkers that correlate with clinical outcome.

Start Date01 Mar 2025

Sponsor / Collaborator

Institut fr Klinische Krebsforschung IKF GmbH

NCT06263153

/ RecruitingPhase 2IIT

A Phase II Trial of Futibatinib in Combination with Durvalumab (MEDI4736) Administered to Cisplatin-Ineligible Patients with Muscle-Invasive Bladder Cancer Before Cystectomy

This phase II trial tests how well the combination of futibatinib and durvalumab given before cystectomy works in treating patients with muscle-invasive bladder cancer (MIBC) who are ineligible for cisplatin-based therapy. Cisplatin-based therapy is the standard of care for patients with MIBC. However, many patients cannot receive standard therapy due to poor renal function, peripheral neuropathy, poor functional status, or clinically significant heart failure. Futibatinib may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. Durvalumab is a monoclonal antibody that may interfere with the ability of tumor cells to grow and spread. Radical cystectomy is a surgery to remove all of the bladder as well as nearby tissues and organs. Giving futibatinib in combination with durvalumab before surgery may be an effective treatment option for patients with MIBC who are ineligible for cisplatin-based therapy.

Start Date30 Dec 2024

Sponsor / Collaborator

Ohio State University Comprehensive Cancer Center

[+1]

CTIS2024-512217-40-00

/ RecruitingPhase 2/3

An Open-label, Rollover Study of Futibatinib in Patients Previously Enrolled in an Antecedent Futibatinib Study - TAS-120-404

Start Date21 Oct 2024

Sponsor / Collaborator

Taiho Oncology, Inc.

100 Clinical Results associated with Futibatinib

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100 Translational Medicine associated with Futibatinib

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100 Patents (Medical) associated with Futibatinib

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143

Literatures (Medical) associated with Futibatinib

01 Apr 2025·MOLECULAR DIVERSITY

Targeting AFP-RARβ complex formation: a potential strategy for treating AFP-positive hepatocellular carcinoma

Article

Author: Dev, Radul R ; Soman, Sowmya ; Banjan, Bhavya ; Raju, Rajesh ; Vishwakarma, Riya ; Rehman, Niyas ; Kalath, Haritha ; Kumar, Pankaj ; Revikumar, Amjesh ; Abhinand, Chandran S ; Ramakrishnan, Krishnapriya

Alpha-fetoprotein (AFP) is a glycoprotein primarily expressed during embryogenesis, with declining levels postnatally. Elevated AFP levels correlate with pathological conditions such as liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Recent investigations underscore AFP's intracellular role in HCC progression, wherein it forms complexes with proteins like Phosphatase and tensin homolog (PTEN), Caspase 3 (CASP3), and Retinoic acid receptors and Retinoid X receptors (RAR/RXR). RAR and RXR regulate gene expression linked to cell death and tumorigenesis in normal physiology. AFP impedes RAR/RXR dimerization, nuclear translocation, and function, promoting gene expression favoring cancer progression in HCC that provoked us to target AFP as a drug candidate. Despite extensive studies, inhibitors targeting AFP to disrupt complex formation and activities remain scarce. In this study, employing protein-protein docking, amino acid residues involved in AFP-RARβ interaction were identified, guiding the definition of AFP's active site for potential inhibitor screening. Currently, kinase inhibitors play a significant role in cancer treatment and, the present study explores the potential of repurposing FDA-approved protein kinase inhibitors to target AFP. Molecular docking with kinase inhibitors revealed Lapatinib as a candidate drug of the AFP-RARβ complex. Molecular dynamics simulations and binding energy calculations, employing Mechanic/Poisson-Boltzmann Surface Area (MM-PBSA), confirmed Lapatinib's stability with AFP. The study suggests Lapatinib's potential in disrupting the AFP-RARβ complex, providing a promising avenue for treating molecularly stratified AFP-positive HCC or its early stages.

01 Apr 2025·ANNALS OF ONCOLOGY

Genomic correlates of response and resistance to the irreversible FGFR1-4 inhibitor futibatinib based on biopsy and circulating tumor DNA profiling

Article

Author: Bridgewater, J A ; Meric-Bernstam, F ; Okamura, S ; Silhavy, J L ; Kano, A ; Hollebecque, A ; Halim, A ; DiToro, D ; Shimura, M ; Wacheck, V ; Goyal, L

BACKGROUND:

Futibatinib is the only covalent inhibitor of FGFR1-4 to gain regulatory approval in oncology. In this article, we present genomic analyses of tissue biopsies and circulating tumor DNA (ctDNA) from patients with 1 of nearly 20 tumor types treated with futibatinib in the phase I/II FOENIX study.

PATIENTS AND METHODS:

Eligible patients included those with ctDNA samples collected per protocol at baseline and/or progression on futibatinib in the phase Ib portion of the study for FGF/FGFR-altered advanced solid tumors or the phase II portion of the study for FGFR2 fusion/rearrangement-positive cholangiocarcinoma. Assessments included analytical concordance between tumor and ctDNA analyses for detection of FGFR alterations, association of ctDNA-detected co-occurring genomic alterations with response to futibatinib, and determination of patterns of acquired resistance following progression on futibatinib.

RESULTS:

Among 300 patients treated with futibatinib, 226 were eligible for this analysis, including 139 (62%) with cholangiocarcinoma. Among patients with known FGFR2 fusions/rearrangements, FGFR1 fusions, FGFR3 fusions, or FGFR2 amplifications per tissue analysis, detection rates in ctDNA for these aberrations were 84%, 0%, 11%, and 59%, respectively. Objective response rates on futibatinib were not significantly different between patients with TP53-altered versus -unaltered solid tumors; progression-free survival was reduced in patients with CDKN2B-altered versus -unaltered cholangiocarcinoma (median 4.8 versus 11.0 months; P = 0.03). Acquired resistance to futibatinib was frequently polyclonal and driven by an array of mutations within the relevant FGFR kinase domain, predominantly V565L, V565F, and N550K variants.

CONCLUSIONS:

In this largest and most systematic analysis of acquired resistance to an FGFR inhibitor from prospective clinical trials, emergence of secondary FGFR2 kinase domain mutations was observed in most patients receiving clinical benefit to futibatinib. ctDNA analysis shows clinically relevant potential as a noninvasive method for assessing genomic profiles, identifying patients who may benefit from FGFR inhibitor treatment, and exploring acquired resistance mechanisms.

01 Mar 2025·EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY

Design, synthesis, and biological evaluation of a potent and orally bioavailable FGFRs inhibitor for fibrotic treatment

Article

Author: Wei, Wei ; Xie, Yuting ; Wu, Xiuli ; Liu, Hongyao ; Tan, Zui ; Ye, Tinghong ; Gan, Cailing ; Su, Xingping ; Xue, Taixiong ; Yue, Lin ; Li, Peilin ; Liu, Zhihao ; Wang, Doudou

Organ fibrosis, such as lung fibrosis and liver fibrosis, is a progressive and fatal disease. Fibroblast growth factor receptors (FGFRs) play an important role in the development and progression of fibrosis. Through scaffold hopping, bioisosteric replacement design, and structure-activity relationship optimization, we developed a series of highly potent FGFRs inhibitors, and the indazole-containing candidate compound A16 showed potent kinase activity comparable to that of AZD4547. In addition, A16 effectively suppressed the activation of lung fibroblasts and hepatic stellate cells (HSCs) induced by TGF-β1, leading to a reduction in collagen deposition. Notably, A16 exhibited potent anti-fibrotic effects through the inhibition of the FGFR pathway in vitro. Compound A16 also showed reasonable pharmacokinetic properties (F = 21.84 %) and favorable cardiac safety (hERG IC₅₀ > 20 μM). Moreover, in models of pulmonary fibrosis, A16 ameliorated (in the prevention model) and reversed (in the treatment model) bleomycin-induced lung fibrosis, as well as mitigated inflammatory immune response in the lung. Furthermore, in the CCl₄-induced liver fibrosis model, when A16 was administrated orally at a dose of 30 mg/kg/day for 3 weeks, it effectively improved liver function, restored damaged liver structures, and reduced collagen deposition. Taken together, these results suggest that A16 could be a potential drug candidate for the treatment of organ fibrosis.

31

News (Medical) associated with Futibatinib

28 Mar 2025

·www.fiercepharma.com

Fierce Pharma Asia—Novo's triple G obesity bet; Merck's latest China deal; Hengrui, Elevar's 2nd FDA snub

Novo Nordisk's China obesity deal, Merck's cardiovascular licensing deal, and an FDA rejection for Hengrui and Elevar's PD-1 combo made our news this week. Novo Nordisk snapped up an obesity asset from China's United Laboratories in a deal worth up to $2 billion. Merck & Co. got a lipoprotein(a) inhibitor from Jiangsu Hengrui Pharma for cardiovascular disease. Hengrui and Elevar Therapeutics' PD-1 liver cancer combination was again tripped up by manufacturing at the FDA.1. Novo Nordisk pens $2B deal for triple G agonist tied to 15% weight loss at 12 weeksNovo Nordisk has bought into the “triple G” idea, gaining a GLP-1/GIP/glucagon triple agonist from China’s United Laboratories for up to $2 billion. The candidate, coded UBT251, would be a direct competitor to Eli Lilly’s retatrutide. In a phase 1b trial, weekly UBT251 at the highest subcutaneous dose of 6 mg led to an average 15.1% weight loss from baseline after 12 weeks.2. Merck & Co. pens $200M upfront deal for Hengrui's midstage heart disease medIn another China deal potentially worth up to $2 billion, Merck & Co. is paying $200 million upfront for a phase 2 lipoprotein(a) inhibitor from Hengrui Pharma. Elevated Lp(a) in the blood, as a risk factor for cardiovascular disease, has become an increasingly popular target. Lilly has a clinical candidate called muvalaplin, and AstraZeneca last year licensed a preclinical one from China’s CSPC Pharma.3. FDA rejects Hengrui, Elevar's PD-1 cancer drug combination—againIn a piece of bad news for Hengrui, the FDA has once again rejected its Elevar Therapeutics-partnered combination of the PD-1 inhibitor camrelizumab and VEGFR inhibitor rivoceranib. Like the first rejection last year, the FDA this time also raised problems with Hengrui’s camrelizumab manufacturing facility in China.4. AbbVie takes Genmab to court, accusing partner of being 'willfully blind' to ADC trade secret theftAbbVie has sued Genmab over the Danish company’s $1.8 billion acquisition of Sino-American biotech ProfoundBio last year. The Illinois pharma alleged that Genmab was “intentionally and willfully blind” to Profound’s alleged theft of its antibody-drug conjugate trade secrets. Genmab said it “categorically refutes allegations and will vigorously defend the company.”5. J&J combo signals new era in EGFR lung cancer with survival win against AstraZeneca's TagrissoJohnson & Johnson’s Rybrevant and its Yuhan-partnered Lazcluze significantly reduced the risk of death by 25% versus AstraZeneca’s Tagrisso in first-line EGFR-mutated non-small cell lung cancer, according to a high-stakes readout from the phase 3 Mariposa trial. J&J believes the overall survival win sets the combo up to be the new standard of care. But the high-maintenance nature of the regimen poses a challenge.6. Drugmakers fear Trump tariffs will drive up manufacturing costs, hurt medicine access: BIO surveyTrump again threatens tariffs on pharmaceuticals in 'not too distant' futurePresident Donald Trump said his administration will announce tariffs on pharmaceuticals “in the not too distant” future. But in a recent survey conducted by the Biotechnology Innovation Organization, a large proportion of biopharma companies polled said tariffs on EU, Canada or China will drive up manufacturing costs. Many respondents also fear that tariffs could disrupt R&D and regulatory plans.7. FDA calls out 'particularly concerning' claims on HCP site for Taiho's LytgobiThe FDA has taken issue with Taiho Oncology’s doctor-facing web page for the cholangiocarcinoma drug Lytgobi. The agency raised concerns that some descriptions of the drug’s overall survival and progression-free survival data from a single-arm phase 2 study were misleading. The agency is giving the firm 15 working days to submit a written response.8. Eisai lays out road map to blockbuster sales projections for Leqembi's 'milestone' 2027 year9. Contractors WuXi Bio, WuXi XDC eye continued growth after logging solid performances in 202410. Gavi terminates COVID vaccine deal with Clover, demands $224M repayment11. Ascletis slashes funding for former core programs in pivot to obesity12. ImmuneOnco axes CD47 bispecific as pipeline prioritization pressures hit Chinese biotech13. India's Aspen Biopharma Labs hit with FDA warning letter citing infrastructure, contamination and records problems14. Biotech designed to commercialize Ascendis' endocrinology drugs in China files $86M IPO15. Bharat Biotech enters cell and gene therapy market with $75M production investment: reports16. Bayer gains Puhe’s cancer drug candidate in another China deal (release)17. Kaken agrees to $180M deal to develop Alumis' lead TYK2 inhibitor in Japan

VaccinePhase 2Phase 1Clinical ResultPhase 3

26 Mar 2025

·endpts.com

FDA critiques Taiho Oncology's 'misleading' promotional website for bile duct cancer drug

The FDA is taking issue with a promotional website from Taiho Oncology, alleging it misleadingly describes the benefits of its bile duct cancer drug Lytgobi, which won accelerated approval in 2022. The untitled letter sent last week calls out the way the company’s website offers allegedly misleading interpretations of efficacy in the single-arm trial on which the accelerated approval was based. The agency said certain efficacy-related parts of the webpage misbrand Lytgobi “by misleadingly suggesting that FOENIX-CCA2,” a Phase 1/2 study in 103 patients , “provided interpretable results regarding the effects of Lytgobi on PFS [progression-free survival] and OS [overall survival] endpoints.” Because FOENIX-CCA2 was designed as a single-arm trial, with no comparator arm, the FDA added, “the reported PFS and OS results are uninterpretable; absent an appropriate comparator, it is not possible to determine if the observed effect is attributable to Lytgobi or to other factor(s), such as the natural history of the disease.” The FDA acknowledged that Taiho said the data presented on its site should be interpreted with caution, but noted that such statements do “not render the promotional communication nonmisleading in light of the issues with FOENIX-CCA2.” Presentations on the website are also “misleading by suggesting that Lytgobi improves DCR [disease control rate] in patients with locally advanced or metastatic iCCA [intrahepatic cholangiocarcinoma] based on a composite of complete response (CR), partial response (PR), and stable disease (SD) when the study from which the presentations were drawn could not demonstrate this result,” the agency said. In a statement to Endpoints News , Taiho said it worked to present data “in a manner that is truthful and not misleading and consistent with FDA guidelines” and was “reviewing their comments and will respond appropriately and in a timely manner.” This is the second untitled letter this year from the FDA’s Office of Prescription Drug Promotion to industry.

Accelerated Approval

17 Mar 2025

·www.fiercebiotech.com

Otsuka\'s Taiho pays $400M for Swiss partner to \'turbocharge\' 3 ADCs to clinic

Taiho Pharmaceutical\'s \"significant cancer expertise will support us in turbocharging the clinical development of our potent ADC candidates in hematological and solid tumors,” Araris Biotech\'s CEO said.\n Otsuka’s Taiho Pharmaceutical is paying $400 million upfront to acquire Switzerland’s Araris Biotech and its antibody-drug conjugate (ADC) linker platform.The two companies have been working together since November 2023, when Araris agreed to use its AraLinQ platform to develop ADCs aimed at Taiho’s targets of choice. Taiho presumably liked what it saw, as the biotech has now decided to go all-in and buy Araris.The deal will see Taiho hand over $400 million, with Araris’ shareholders potentially in line for a further $740 million in milestone payments, according to a March 17 release.Araris has its origins in Switzerland’s Paul-Scherrer-Institute, before spinning off in 2019. The biotech is focused on designing ADCs that have greater linker solubility, with three preclinical therapies aimed at hematological and solid tumors expected to enter human trials over the course of 2025 and 2026.Araris touts its linker tech as having three benefits over its competitors. Firstly, the attachment site on a specific amino acid within the antibody IgG-Fc framework means the antibody maintains almost the same performance when part of the ADC. Meanwhile, the strong peptide bond connecting the linker antibody to the therapy’s payload results in “exceptional stability in the blood stream and therefore, avoidance of healthy tissue damage,” according to the release. This bond then breaks easily inside a cancer cell.“Araris’ unique ADC technology represents a quantum leap for the ADC field, potentially offering precise payload delivery of multiple mechanisms of action simultaneously to the tumor, with less toxicity,” CEO and co-founder Dragan Grabulovski said. “We are proud to combine with Taiho, our partner since November 2023, whose significant cancer expertise will support us in turbo-charging the clinical development of our potent ADC candidates in hematological and solid tumors.”Taiho is a subsidiary of Japan’s Otsuka and markets a wide range of anticancer drugs in the country. In the U.S., the subsidiary has three FDA-approved products: the colorectal treatment Lonsurf, the bile duct cancer med Lytgobi and the myelodysplastic syndromes treatment Inqovi.Using Araris’ ADC drug tech alongside Taiho’s own small-molecule drug discovery platform Cysteinomix will allow Taiho to “further expand its ongoing development portfolio in the field of oncology,” according to this morning’s release.ADCs have been one of the hottest spaces for dealmaking in recent years, with the likes of AstraZeneca, Roche, Merck & Co. and Ipsen all posting billion-dollar-plus biobucks pacts.

$Otsuka\'s Taiho pays $400M for Swiss partner to \'turbocharge\' 3 ADCs to clinic$

ADCDrug ApprovalAcquisition

100 Deals associated with Futibatinib

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External Link

KEGG	Wiki	ATC	Drug Bank
D11725	-	-	DB15149

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
FGFR2 fusion or rearranged Cholangiocarcinoma	Japan	Taiho Pharmaceutical Co., Ltd.	26 Jun 2023
Intrahepatic Cholangiocarcinoma	United States	Taiho Oncology, Inc.	30 Sep 2022

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Biliary Tract Neoplasms	NDA/BLA	Japan	Taiho Pharmaceutical Co., Ltd.	30 Jan 2022
Neoplasm Metastasis	Phase 3	United States	Taiho Oncology, Inc.	01 Oct 2024
Neoplasm Metastasis	Phase 3	France	Taiho Oncology, Inc.	01 Oct 2024
Neoplasm Metastasis	Phase 3	Spain	Taiho Oncology, Inc.	01 Oct 2024
Neoplasm Metastasis	Phase 3	United Kingdom	Taiho Oncology, Inc.	01 Oct 2024
Adenocarcinoma of Esophagus	Phase 2	United States	Taiho Oncology, Inc.	13 Jul 2023
Adenocarcinoma of Esophagus	Phase 2	France	Taiho Oncology, Inc.	13 Jul 2023
Adenocarcinoma of Esophagus	Phase 2	Germany	Taiho Oncology, Inc.	13 Jul 2023
Adenocarcinoma of Esophagus	Phase 2	Spain	Taiho Oncology, Inc.	13 Jul 2023
Esophageal Squamous Cell Carcinoma	Phase 2	United States	Taiho Oncology, Inc.	13 Jul 2023

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Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04093362 (FOENIX-CCA3, CTgov)	Phase 3	FGFR2 fusion or rearranged Cholangiocarcinoma	10	Futibatinib	eiegcilyzz = rvyeafmxii zdgjgtpjsb (tlmgbscveo, dmbuoirywa - wtjeubozgf) View more	-	07 Feb 2025
NCT04999761 (ASCO_GI2025) Manual	Phase 1	Metastatic Esophageal Carcinoma First line	43	Zimberelimab + Futibatinib + cisplatin + fluorouracil	hoisaippwf(wedbnttjpn) = DLTs were evaluated in the first three pts, and none were reported. zaxarcsqmg (sfosvbpyfz )	Positive	23 Jan 2025
Phase 1b study of futibatinib plus pembrolizumab (ASCO_GI2025)	Phase 1	Esophageal Carcinoma CD3+ \| CD4 \| CD8+ ... View more	18	Futibatinib + Pembrolizumab	dtflxyyhou(tlgiwvxfkn) = 22.2% bnibpjpksb (sivyfvptiu ) View more	Positive	23 Jan 2025
NCT04601857 (ESMO2024) Manual	Phase 2	Transitional Cell Carcinoma First line FGFR alteration	43	Futibatinib 20 mg PO QD Pembrolizumabzumab 200 mg IV Q3W	sywlyldzxt(ihwgwdwulm) = idyyuxcxwc vrylkaeaeh (fufcuyhfpq, 23 - 72) View more	Positive	15 Sep 2024
NCT04601857 (ESMO2024) Manual	Phase 2	Transitional Cell Carcinoma First line FGFR alteration	43	Futibatinib 20 mg PO QD+PembrolizumabPembrolizumab 200 mg IV Q3W (without FGFR3 mutations or FGFR1–4 fusion/rearrangements)	sywlyldzxt(ihwgwdwulm) = gbauhfhclw vrylkaeaeh (fufcuyhfpq, 14 - 52) View more	Positive	15 Sep 2024
NCT02052778 (FOENIX-CCA2, Pubmed \| Future Oncol) Manual	Phase 2	Advanced Bile Duct Carcinoma FGFR2 Fusion	-	Futibatinib	pcplibzqzw(tgwzcwhccu) = upicuymcdm eruwpbhpto (myrnbtyiel ) View more	Positive	17 Jun 2024
JPRN-jRCT2080224975 (ASCO2024) Manual	Phase 1	Esophageal Carcinoma	-	Futibatinib 2Pembrolizumabembrolizumab 200mg/q3w with chemotherapy	gpiiqwexoc(ltceyciiqt) = nvxudeezwq habjcvaowg (muqzaecedm, 43.4 - 87.4) View more	Positive	24 May 2024
JPRN-jRCT2080224975 (ASCO2024) Manual	Phase 1	Esophageal Carcinoma	-	Futibatinib 20Pembrolizumabmbrolizumab 200mg/q3w without chemotherapy	gpiiqwexoc(ltceyciiqt) = nyiqzqmdfz habjcvaowg (muqzaecedm, 26.3 - 60.6) View more	Positive	24 May 2024
JPRN-jRCT2080224975 (ESMO 12023 \| ESMO 22023) Manual	Phase 1	Esophageal Carcinoma	92	Futibatinib + pembrolizumab (ICI naïve)	pevfomkoyi(akwaabxkwr) = ymmyehfays wlrzcjuquw (aimfwgpsnr ) View more	Positive	23 Oct 2023
JPRN-jRCT2080224975 (ESMO 12023 \| ESMO 22023) Manual	Phase 1	Esophageal Carcinoma	92	Futibatinib + pembrolizumab (ICI refractory)	pevfomkoyi(akwaabxkwr) = vxgajliqau wlrzcjuquw (aimfwgpsnr ) View more	Positive	23 Oct 2023
TAS-120-101 (EMA) Manual	Not Applicable	FGFR2 fusion or rearranged Cholangiocarcinoma	103	futibatinib	hwnaztpvsu(myxakyjwjk) = bkowmmdoty jzzbkximal (perntxfsct, 32 - 52) View more	Positive	18 Jul 2023
NCT04189445 (SO-10, ESMO_GI2023)	Phase 2	FGFR2 positive Gastrooesophageal Junction Cancer FGFR2 amplification	28	Futibatinib 20 mg	jfhxcetfys(zbydtewzzn) = asvrmrkfkl zokufjlrxe (grrwwvgole, 6.1 - 36.9) View more	Positive	01 Jul 2023
NCT02052778 (FOENIX-CCA2, ESMO_GI2023)	Phase 2	FGFR2 positive Intrahepatic Cholangiocarcinoma FGFR2	103	Futibatinib	elhmzfdhmk(lbarxxbhie) = rjddvsvytz jpygxxmhly (pxymplbmtw ) View more	Positive	01 Jul 2023