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

NeoplasmsOther DiseasesDigestive System Disorders+ [3]

Active Indication

FGFR2 fusion or rearranged CholangiocarcinomaIntrahepatic CholangiocarcinomaBiliary Tract Neoplasms+ [12]

Inactive Indication

Advanced Malignant Solid NeoplasmCentral Nervous System NeoplasmsKRAS Mutant Pancreatic Cancer+ [3]

Originator Organization

Taiho Pharmaceutical Co., Ltd.

Active Organization

Taiho Oncology, Inc.

Taiho Pharmaceutical Co., Ltd.

Mayo Clinic

Inactive Organization-

Drug Highest PhaseApproved

First Approval Date

US (30 Sep 2022),

Intrahepatic Cholangiocarcinoma

RegulationPriority Review (US), Breakthrough Therapy (US), Accelerated Approval (US), Orphan Drug (US), Orphan Drug (EU), Orphan Drug (AU), Conditional marketing approval (EU)

Structure

Molecular FormulaC22H22N6O3

InChIKeyKEIPNCCJPRMIAX-HNNXBMFYSA-N

CAS Registry1448169-71-8

Clinical Trials associated with Futibatinib

NCT06263153 / Not yet recruitingPhase 2

A Phase II Trial of Futibatinib in Combination With Durvalumab 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 Date01 Jun 2024

Sponsor / Collaborator

Ohio State University Comprehensive Cancer Center

[+1]

NCT05615818 / RecruitingPhase 3

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 Date29 May 2024

Sponsor / Collaborator

UNICANCER

[+8]

NCT05945823 / RecruitingPhase 2

A Phase 2 Study of Futibatinib in Combination With PD-1 Antibody-based Standard of Care Therapy in Patients With Solid Tumors.

This is a nonrandomized, uncontrolled, open-label, multicenter Phase 2 study to evaluate the efficacy, safety, and tolerability of futibatinib in combination with PD-1 antibody-based SoC therapy in adult patients with solid tumors.

Start Date13 Jul 2023

Sponsor / Collaborator

Taiho Oncology, Inc.

100 Clinical Results associated with Futibatinib

100 Translational Medicine associated with Futibatinib

100 Patents (Medical) associated with Futibatinib

Literatures (Medical) associated with Futibatinib

01 Feb 2024·Current medicinal chemistry

Futibatinib: A Potent and Irreversible Inhibitor of Fibroblast Growth Factor Receptors for Treatment of the Bile Duct Cancer

Article

Author: De, Surya K

Abstract::

Cholangiocarcinoma is a rare type of cancer. Futibatinib is an irreversible, potent, selective inhibitor of fibroblast growth factor receptors (FGFR 1-4). On September 30, 2022, the US FDA first approved futibatinib to treat adult patients with bile duct cancer whose disease is unresectable, locally advanced, or metastatic intrahepatic cholangiocarcinoma harboring fibroblast growth factor receptor 2 (FGFR2) gene mutations or other classes of rearrangements. The approval of this medicine was based on phase 3 clinical trial results including an overall response rate (ORR) of 42% and a duration of response (DoR) of 9.7 months. This short perspective summarizes Futibatinib’s synthesis, physicochemical properties, dosage, route of administration, mechanism of action, binding mode, pharmacodynamics, pharmacokinetics, drug interactions, adverse events, and possible mechanism of resistance.

01 Feb 2024·Journal of hepatology

Convergent MAPK pathway alterations mediate acquired resistance to FGFR inhibitors in FGFR2 fusion-positive cholangiocarcinoma

Article

Author: Lee, Sunyoung S ; Javle, Milind ; Zhao, Ming ; Kahle, Michael P ; Scott, Stephen ; Wacheck, Volker ; DiPeri, Timothy P ; Rodon, Jordi ; Halim, Abdel-Baset ; Hirai, Hiroshi ; Moss, Tyler ; Chen, Huiqin ; Kwong, Lawrence N ; Byrnes, Charnel C ; Evans, Kurt W ; Meric-Bernstam, Funda ; Varadarajan, Kaushik

BACKGROUND & AIMS:

There is a knowledge gap in understanding mechanisms of resistance to fibroblast growth factor receptor (FGFR) inhibitors (FGFRi) and a need for novel therapeutic strategies to overcome it. We investigated mechanisms of acquired resistance to FGFRi in patients with FGFR2-fusion-positive cholangiocarcinoma (CCA).

METHODS:

A retrospective analysis of patients who received FGFRi therapy and underwent tumor and/or cell-free DNA analysis, before and after treatment, was performed. Longitudinal circulating tumor DNA samples from a cohort of patients in the phase I trial of futibatinib (NCT02052778) were assessed. FGFR2-BICC1 fusion cell lines were developed and secondary acquired resistance mutations in the mitogen-activated protein kinase (MAPK) pathway were introduced to assess their effect on sensitivity to FGFRi in vitro.

RESULTS:

On retrospective analysis of 17 patients with repeat sequencing following FGFRi treatment, new FGFR2 mutations were detected in 11 (64.7%) and new alterations in MAPK pathway genes in nine (52.9%) patients, with seven (41.2%) patients developing new alterations in both the FGFR2 and MAPK pathways. In serially collected plasma samples, a patient treated with an irreversible FGFRi tested positive for previously undetected BRAF V600E, NRAS Q61K, NRAS G12C, NRAS G13D and KRAS G12K mutations upon progression. Introduction of a FGFR2-BICC1 fusion into biliary tract cells in vitro sensitized the cells to FGFRi, while concomitant KRAS G12D or BRAF V600E conferred resistance. MEK inhibition was synergistic with FGFRi in vitro. In an in vivo animal model, the combination had antitumor activity in FGFR2 fusions but was not able to overcome KRAS-mediated FGFRi resistance.

CONCLUSIONS:

These findings suggest convergent genomic evolution in the MAPK pathway may be a potential mechanism of acquired resistance to FGFRi.

CLINICAL TRIAL NUMBER:

NCT02052778.

IMPACT AND IMPLICATIONS:

We evaluated tumors and plasma from patients who previously received inhibitors of fibroblast growth factor receptor (FGFR), an important receptor that plays a role in cancer cell growth, especially in tumors with abnormalities in this gene, such as FGFR fusions, where the FGFR gene is fused to another gene, leading to activation of cancer cell growth. We found that patients treated with FGFR inhibitors may develop mutations in other genes such as KRAS, and this can confer resistance to FGFR inhibitors. These findings have several implications for patients with FGFR2 fusion-positive tumors and provide mechanistic insight into emerging MAPK pathway alterations which may serve as a therapeutic vulnerability in the setting of acquired resistance to FGFRi.

05 Jan 2024·Clinical cancer research : an official journal of the American Association for Cancer Research

Landscape of Clinical Resistance Mechanisms to FGFR Inhibitors in FGFR2-Altered Cholangiocarcinoma

Article

Author: Ellis, Haley ; Fece de la Cruz, Ferran ; Bardeesy, Nabeel ; Norden, Bryanna L. ; Che, Jianwe ; Michel, Alexa G. ; Silveira, Vanessa S. ; Corcoran, Ryan B. ; Siravegna, Giulia ; Balasooriya, Eranga Roshan ; Zhen, Yuanli ; Wu, Qibiao

Abstract:

Purpose::

FGFR inhibitors are effective in FGFR2-altered cholangiocarcinoma, leading to approval of reversible FGFR inhibitors, pemigatinib and infigratinib, and an irreversible inhibitor, futibatinib. However, acquired resistance develops, limiting clinical benefit. Some mechanisms of resistance have been reported, including secondary FGFR2 kinase domain mutations. Here, we sought to establish the landscape of acquired resistance to FGFR inhibition and to validate findings in model systems.

Experimental Design::

We examined the spectrum of acquired resistance mechanisms detected in circulating tumor DNA or tumor tissue upon disease progression following FGFR inhibitor therapy in 82 FGFR2-altered cholangiocarcinoma patients from 12 published reports. Functional studies of candidate resistance alterations were performed.

Results::

Overall, 49 of 82 patients (60%) had one or more detectable secondary FGFR2 kinase domain mutations upon acquired resistance. N550 molecular brake and V565 gatekeeper mutations were most common, representing 63% and 47% of all FGFR2 kinase domain mutations, respectively. Functional studies showed different inhibitors displayed unique activity profiles against FGFR2 mutations. Interestingly, disruption of the cysteine residue covalently bound by futibatinib (FGFR2 C492) was rare, observed in 1 of 42 patients treated with this drug. FGFR2 C492 mutations were insensitive to inhibition by futibatinib but showed reduced signaling activity, potentially explaining their low frequency.

Conclusions::

These data support secondary FGFR2 kinase domain mutations as the primary mode of acquired resistance to FGFR inhibitors, most commonly N550 and V565 mutations. Thus, development of combination strategies and next-generation FGFR inhibitors targeting the full spectrum of FGFR2 resistance mutations will be critical.

News (Medical) associated with Futibatinib

13 May 2024

·www.biospace.com

Boundless Bio Reports First Quarter 2024 Financial Results and Corporate Highlights

BBI-355 Phase 1/2 POTENTIATE clinical trial ongoing; initiated targeted therapy combinations in patients with tumors with EGFR or FGFR oncogene amplifications First patient dosed in Phase 1/2 STARMAP clinical trial of BBI-825 in patients with tumors with resistance gene amplifications Completed $100 million IPO; pro forma cash position of approximately $200 million supports both BBI-355 and BBI-825 through preliminary clinical proof of concept SAN DIEGO--(BUSINESS WIRE)-- Boundless Bio (Nasdaq: BOLD), a clinical-stage oncology company interrogating extrachromosomal DNA (ecDNA) biology to deliver transformative therapies to patients with previously intractable oncogene amplified cancers, today announced financial results for the first quarter of 2024 and highlighted recent progress. “It has been an exciting quarter at Boundless Bio. The Phase 1/2 POTENTIATE trial of BBI-355, our potentially best-in-class, oral, selective CHK1 inhibitor, advanced into initial combination therapy modules evaluating BBI-355 together with an EGFR inhibitor or an FGFR inhibitor in patients with tumors harboring EGFR or FGFR oncogene amplifications, respectively. We also dosed the first patient with our second ecDNA-directed therapy (ecDTx), BBI-825, a first-in-class, oral, selective RNR inhibitor, which marks the company’s rapid growth and transition into a multi-asset, clinical-stage oncology company” said Zachary Hornby, President and Chief Executive Officer of Boundless Bio. “With the completion of our recent IPO, we have the capital to take the next steps toward delivering on the promise of our ecDTx, a potential new vertical in cancer therapeutics.” Recent Highlights BBI-355, a novel CHK1 inhibitor and the first ecDTx in development Patient enrollment is ongoing in Part 1 of the Phase 1/2 POTENTIATE (Precision Oncology Trial Evaluating Novel Therapeutic Interrupting Amplifications Tied to ecDNA) trial, which evaluates BBI-355 as a single agent in patients with locally advanced or metastatic solid tumors with oncogene amplifications. Initiated dose escalation in Part 2 of the Phase 1/2 POTENTIATE trial, which evaluates BBI-355 in combination with the EGFR inhibitor erlotinib and BBI-355 in combination with the FGFR inhibitor futibatinib in patients with tumors harboring EGFR or FGFR oncogene amplifications, respectively, to evaluate the safety, tolerability, pharmacokinetics, and preliminary antitumor activity of each combination regimen. Presented preliminary preclinical and clinical pharmacodynamic data on BBI-355 at the American Association for Cancer Research (AACR) Annual Meeting 2024. Findings further support the development of BBI-355 as a differentiated single agent and combination treatment approach for oncogene amplified cancers. BBI-825, a novel, selective RNR inhibitor targeting ecDNA assembly and repair Dosed the first patient in the STARMAP (Study Targeting Acquired Resistance: MAPK Amplifications) trial, a first-in-human, Phase 1/2 study of BBI-825 as a single agent and in combination with select targeted cancer therapies, for patients with locally advanced or metastatic cancer with resistance gene amplifications. First Quarter 2024 Financial Highlights Cash Position: Cash, cash equivalents, and short-term investments totaled $104.9 million as of March 31, 2024. In addition, Boundless Bio completed its IPO in early April 2024 in which it sold 6,250,000 shares of its common stock for gross proceeds of $100.0 million. Boundless Bio expects its current cash position to fund operations into the second half of 2026 and through key clinical data milestones. R&D Expenses: Research and development (R&D) expenses were $13.1 million for the first quarter of 2024, compared to $9.5 million for the same period in 2023. The increase in R&D expenses was primarily due to a $1.8 million increase in the direct program costs for BBI-355, BBI-825, and other development programs, a $0.5 million increase in personnel-related costs resulting from an increase in headcount and salary increases, $0.3 million of additional stock-based compensation, and a $1.0 million increase in third-party services and other miscellaneous R&D costs. G&A Expenses: General and administrative (G&A) expenses were $3.8 million for the first quarter of 2024, compared to $2.6 million for the same period in 2023. The increase in G&A expenses was primarily due to a $0.3 million increase in personnel-related costs due to an increase in headcount and salary increases, $0.5 million of additional stock-based compensation, an increase in professional service fees of $0.2 million, and a $0.2 million increase in other G&A costs. Net Loss: Net loss totaled $15.4 million and $11.7 million for the first quarters of 2024 and 2023, respectively, with non-cash stock-based compensation expense of $1.3 million and $0.6 million for the first quarters of 2024 and 2023, respectively. About BBI-355 Boundless Bio’s lead ecDNA-directed therapy (ecDTx), BBI-355, is a novel, oral, selective small molecule inhibitor of checkpoint kinase 1 (CHK1) being studied in the ongoing, first-in-human, Phase 1/2 POTENTIATE clinical trial (NCT05827614) in patients with oncogene amplified cancers. CHK1 is a master regulator of cells’ response to replication stress (RS). RS is elevated in ecDNA-enabled oncogene amplified cancer cells and, because of this, represents a key vulnerability of those cells. BBI-355 was designed to exploit the elevated RS in ecDNA-enabled oncogene amplified cancer cells by disrupting proper CHK1 function in regulating RS and thereby facilitating catastrophic RS to preferentially kill cancer cells relative to healthy cells. About BBI-825 Boundless Bio’s second ecDTx, BBI-825, is a novel, oral, selective small molecule inhibitor of ribonucleotide reductase (RNR) being studied in the ongoing, first-in-human, Phase 1/2 STARMAP clinical trial (NCT06299761) in cancer patients with resistance gene amplifications. In preclinical studies, BBI-825 demonstrated low double digit nanomolar RNR inhibition and tumor growth inhibition, including regressions, in both the prevention and treatment of amplification-mediated resistance in mitogen-activated protein kinase (MAPK) pathway-activated tumors. RNR is the rate-limiting enzyme responsible for cellular de novo synthesis of deoxynucleotide triphosphates (dNTPs), the building blocks of DNA, and is essential to the assembly and repair of ecDNA. BBI-825 was shown to dysregulate ecDNA-reliant cancer cell dNTP pools, deplete ecDNA, and was synthetic lethal in multiple oncogene amplified preclinical cancer models. About Boundless Bio Boundless Bio is a clinical-stage oncology company dedicated to unlocking a new paradigm in cancer therapeutics to address the significant unmet need of patients with oncogene amplified tumors by targeting extrachromosomal DNA (ecDNA), a root cause of oncogene amplification observed in more than 14% of cancer patients. Boundless Bio is developing the first ecDNA-directed therapy (ecDTx), BBI-355, which is an oral inhibitor of checkpoint kinase 1 (CHK1) being evaluated in a Phase 1/2 clinical trial in patients with oncogene amplified cancers. Boundless Bio’s second ecDTx, BBI-825, is an oral inhibitor of ribonucleotide reductase (RNR) being evaluated in a Phase 1/2 clinical trial in cancer patients with resistance gene amplifications. Leveraging its Spyglass platform, Boundless Bio has additional programs advancing through preclinical development and discovery. Boundless Bio is headquartered in San Diego, CA. For more information, visit . Follow us on LinkedIn and X. Forward-Looking Statements Boundless Bio cautions you that statements contained in this press release regarding matters that are not historical facts are forward-looking statements. The forward-looking statements are based on our current beliefs and expectations and include but are not limited to: the sufficiency of our cash position to fund operations and milestones; and the potential therapeutic benefits of our ecDTx in treating patients with oncogene amplified cancers. Actual results may differ from those set forth in this press release due to the risks and uncertainties inherent in our business, including, without limitation: we are early in our development efforts and our approach to discover and develop ecDTx directed against ecDNA in oncogene amplified cancers is novel and unproven; results from preclinical studies or early clinical trials not necessarily being predictive of future results; potential delays in the commencement, enrollment, data readouts or completion of clinical trials or preclinical studies; our dependence on third parties in connection with clinical trials, preclinical studies, ecDNA diagnostic development, and manufacturing; unfavorable results from clinical trials or preclinical studies; unexpected adverse side effects or inadequate efficacy of our ecDTx that may limit their development, regulatory approval, and/or commercialization; the potential for our programs and prospects to be negatively impacted by developments relating to our competitors, including the results of studies or regulatory determinations relating to our competitors; regulatory developments in the United States and foreign countries; we may use our capital resources sooner than we expect; and other risks described in our filings with the Securities and Exchange Commission (SEC), including under the heading “Risk Factors” in our quarterly report on Form 10-Q for the quarter ended March 31, 2024 and any subsequent filings with the SEC. You are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof, and we undertake no obligation to update such statements to reflect events that occur or circumstances that exist after the date hereof. All forward-looking statements are qualified in their entirety by this cautionary statement, which is made under the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. BOUNDLESS BIO, INC. Condensed Statements of Operations (unaudited) (In thousands, except per share amounts) Three Months Ended March 31, 2024 2023 Operating expenses: Research and development $ 13,129 $ 9,503 General and administrative 3,754 2,584 Total operating expenses 16,883 12,087 Loss from operations (16,883 ) (12,087 ) Other income (expense): Interest income 1,421 395 Other income (expense) 32 (27 ) Total other income, net 1,453 368 Net loss $ (15,430 ) $ (11,719 ) Net loss per share, basic and diluted $ (12.27 ) $ (9.91 ) Shares used in calculation 1,258 1,183 BOUNDLESS BIO, INC. Condensed Balance Sheets (In thousands, except par value data) March 31, 2024 December 31, 2023 (unaudited) Assets Current assets Cash and cash equivalents $ 25,143 $ 23,706 Short-term investments 79,737 97,046 Prepaid expenses and other current assets 7,281 3,452 Total current assets 112,161 124,204 Property and equipment, net 2,418 2,573 Right-of-use asset, net 1,385 2,002 Restricted cash 560 560 Other assets 553 555 Total assets $ 117,077 $ 129,894 Liabilities, convertible preferred stock, and stockholders’ deficit Current liabilities Accounts payable and accrued liabilities $ 8,182 $ 4,266 Accrued compensation 939 2,898 Lease liabilities, current portion 1,523 2,195 Total current liabilities 10,644 9,359 Convertible preferred stock 247,617 247,617 Stockholders’ equity: Common stock, $0.0001 par value — — Additional paid-in-capital 10,376 8,987 Accumulated other comprehensive income / (loss) (21 ) 40 Accumulated deficit (151,539 ) (136,109 ) Total stockholders’ deficit (141,184 ) (127,082 ) Total liabilities, convertible preferred stock, and stockholders’ deficit $ 117,077 $ 129,894 View source version on businesswire.com: Contacts James Lee, Boundless Bio jlee@boundlessbio.com Investors THRUST Strategic Communications Renee Leck renee@thrustsc.com Media 1AB Dan Budwick dan@1abmedia.com Source: Boundless Bio View this news release online at:

Financial StatementAACRClinical StudyPhase 1Clinical Result

18 Sep 2023

·www.biospace.com

Boundless Bio Announces Clinical Trial Collaboration and Supply Agreement with Taiho Oncology to Evaluate LYTGOBI® (futibatinib) in Combination with BBI-355 in Patients with FGFR Amplified Solid Tumors

Combination of BBI-355 and futibatinib to be evaluated in Boundless Bio’s ongoing Phase 1/2 clinical trial (POTENTIATE) in patients with FGFR amplifications SAN DIEGO--(BUSINESS WIRE)-- Boundless Bio, a clinical stage, next-generation precision oncology company interrogating extrachromosomal DNA (ecDNA) biology to deliver transformative therapies to patients with previously intractable oncogene amplified cancers, today announced that it has entered into a clinical trial collaboration and supply agreement with Taiho Oncology, Inc. (Taiho) for Taiho’s pan-FGFR inhibitor LYTGOBI® (futibatinib) for use in combination with BBI-355 in a clinical trial of patients with locally advanced or metastatic solid tumors with oncogene amplifications. BBI-355 is an orally administered, novel, selective small molecule inhibitor of CHK1 and represents what Boundless Bio believes is the first ecDNA-directed therapy (ecDTx) in development for oncogene amplified cancers. “This clinical trial collaboration and supply agreement with Taiho marks an important step in the continued execution of our clinical strategy and the next step in realizing the transformative potential of BBI-355, which we believe is the first ecDNA-directed therapy in development for patients with cancer that harbor oncogene amplifications on ecDNA,” said Zachary Hornby, President and Chief Executive Officer of Boundless Bio. “FGFR inhibitors given as monotherapy have to date demonstrated less clinical benefit in patients with cancer harboring FGFR amplifications than in patients with other FGFR driver alteration types. We believe that BBI-355, when combined with Taiho’s futibatinib, has the potential to demonstrate meaningful anti-tumor activity for patients with cancer and FGFR amplifications. We look forward to assessing this novel combination in our ongoing Phase 1/2 POTENTIATE trial.” Under the terms of the agreement, Taiho will provide futibatinib clinical drug supply at no cost for Boundless Bio’s ongoing Phase 1/2 clinical trial (POTENTIATE), which will assess BBI-355 in combination with certain selected targeted therapies, including futibatinib, in patients with specific oncogene amplified solid tumors. About the POTENTIATE Trial BBI-355 is being evaluated in a first-in-human Phase 1/2 clinical trial (“POTENTIATE”: Precision Oncology Trial Evaluating Novel Therapeutic Interrupting Amplifications Tied to ecDNA) in patients with locally advanced or metastatic solid tumors with oncogene amplifications, whose disease has progressed despite all standard therapies or for whom no further standard or clinically acceptable therapy exists. The open-label, non-randomized, 3-part trial involves: BBI-355 single agent dose escalation and expansion in cancer patients with oncogene amplification, dose escalation of BBI-355 in combination with certain selected targeted therapies in cancer patients with specific oncogene amplifications, and dose expansion of BBI-355 in combination with certain selected targeted therapies in cancer patients with specific oncogene amplification on ecDNA. BBI-355 is administered orally every other day. In part 3 of the trial, an ecDNA diagnostic clinical trial assay (CTA), which we call ECHO (ecDNA Harboring Oncogenes), will be implemented to determine the presence of oncogenes amplified on ecDNA in patient tumor samples. ECHO is a proprietary bioinformatic diagnostic algorithm designed by Boundless Bio and developed into a CTA in collaboration with SOPHiA GENETICS to detect oncogenes amplified on ecDNA from tumor biopsy samples using routine clinical NGS assays. About BBI-355 BBI-355 is an orally administered, novel, selective checkpoint kinase 1 (CHK1) inhibitor and, what we believe, is the first ecDNA-directed therapy (ecDTx) being investigated to treat patients with oncogene amplified cancer. CHK1 is a master regulator of the cellular response to DNA replication stress (RS), which frequently arises from oncogene amplification on ecDNA. By disrupting proper CHK1 function in oncogene amplified cancer cells, we believe BBI-355 facilitates catastrophic RS, and preferentially kills cancer cells relative to healthy cells. CHK1 was identified as an ecDNA essential target via Boundless Bio’s proprietary Spyglass research platform. About Boundless Bio Boundless Bio is a clinical stage, next-generation precision oncology company dedicated to the discovery and development of new drugs targeting a novel area of cancer biology, extrachromosomal DNA (ecDNA), to deliver transformative therapies intended to improve and extend the lives of patients with oncogene amplified cancers. Boundless Bio is developing what it believes is the first ecDNA-directed therapy (ecDTx), BBI-355, which is being evaluated in a Phase 1/2 clinical trial and has multiple other pipeline programs advancing in preclinical development and discovery. To date, Boundless Bio has raised more than $250 million from leading life sciences investors. For more information, visit . Follow us on LinkedIn and Twitter. Lytgobi® is a registered trademark of Taiho Pharmaceutical Co., Ltd.

Clinical StudyLicense out/in

07 Sep 2023

·www.prnewswire.com

Acutis Biosciences' CSO Dr. Abdel Halim Co-Authors a Precision Medicine Study in NEJM

Highlights the value of companion diagnostics in the drug industry and the effectiveness of ctDNA testing in blood samples instead of invasive tumor biopsies for patient screening in clinical trials, The assay demonstrated ctDNA liquid biopsy can be an alternative or complement to tissue samples and decrease sample failure rate, Laboratory Developed Test (LDT) results demonstrated the assay was effective for patient selection and qualitative research indicated the value of ctDNA samples versus FFPE tissues. MONMOUTH JUNCTION, N.J., Sept. 7, 2023 /PRNewswire/ -- Dr. Abdel Halim, Acutis Biosciences' Chief Scientific Officer, one of a group who led the study FOENIX-CCA2 (funded by Taiho Oncology and Taiho Pharmaceutical), recently published results about Futibatinib (LYTGOBI®) in cholangiocarcinoma with FGFR2 gene rearrangements/fusions in the New England Journal of Medicine (NEJM). Continue Reading Study demonstrates the clinical value of circulating tumor DNA (ctDNA) in molecular profiling. Tweet this Acutis Bioscience precision medicine study highlights the value of companion diagnostics in the drug industry and the effectiveness of ctDNA testing in blood samples instead of invasive tumor biopsies for patient screening in clinical trials. The study, a multinational phase 2 trial, enrolled patients with FGFR2 fusion/rearrangement–positive unresectable or metastatic intrahepatic cholangiocarcinoma who progressed after one or more previous lines of systemic therapy. Patients were selected based on FGFR2 gene rearrangement/fusion in tumor tissue or liquid biopsy. Dr. Halim was responsible for ensuring the clinical trial assay (CTA) analytical validity and clinical utility in patient selection and addressing laboratory day-to-day issues. The study demonstrated the clinical value of circulating tumor DNA (ctDNA) in molecular profiling to assess patient's eligibility for targeted therapeutics. "It can be an alternative or, at least, complement to tissue samples when those are not available. Using ctDNA testing in blood samples avoids invasive procedures for patients and decreases the analytical sample failure rate caused by insufficient quantity or quality of tissue biopsy. With ctDNA blood samples you are guaranteed as low as 1% failure rate compared to tumor tissues" said Dr. Halim. Dr. Halim's outstanding expertise in the biomarker and precision medicine field brought him to lead biomarkers, translational medicine and precision medicine in 150+ PI-PIII clinical trials for more than 50 drug therapeutic areas, including 12 end-to-end companion diagnostic (CDx) projects on NGS, IHC and PCR, and enabling biomarker-driven patient selection in 35+ early phase trials using lab-developed-tests (LDTs). He is one of only four lab professionals in the USA with triple-board certification in Molecular Diagnostics, Clinical Chemistry and Toxicology, and licensed as CLIA clinical lab director in NY, NJ, FL and TN in several specialties. He is also an accredited FDA third-party reviewer of 510(K) for the different classes of IVDs. Acutis CEO Jibreel Sarij added, "Dr. Halim and his team are making significant impact to bring forward clinical research testing and genomic profiling to enable biopharma with deeper insights and transform precision medicine". About Acutis Bioscience: Acutis Biosciences is a biomarker discovery provider to biopharmaceutical companies with next-generation multi-omics biomarker analysis solutions powered by machine learning (ML) and AI. With technology platforms in genomics and histopathology for development and validation of state-of-the-art cancer molecular diagnostic assays, in oncology, immuno-oncology and infectious diseases, Acutis redefines conventions with a unique customer engagement model coupled to extraordinary science. More info: For more information: Troy Tremaine Chief Commercial Officer Senior Vice President [email protected] SOURCE Acutis Diagnostics Inc.

Phase 2Clinical Result

100 Deals associated with Futibatinib

External Link

KEGG	Wiki	ATC	Drug Bank
D11725	-	-	DB15149

R&D Status

Approved

10 top approved records.

to view more data

Indication	Country/Location	Organization	Date
FGFR2 fusion or rearranged Cholangiocarcinoma	EU	Taiho Pharmaceutical Co., Ltd.	04 Jul 2023
FGFR2 fusion or rearranged Cholangiocarcinoma	IS	Taiho Pharmaceutical Co., Ltd.	04 Jul 2023
FGFR2 fusion or rearranged Cholangiocarcinoma	LI	Taiho Pharmaceutical Co., Ltd.	04 Jul 2023
FGFR2 fusion or rearranged Cholangiocarcinoma	NO	Taiho Pharmaceutical Co., Ltd.	04 Jul 2023
Intrahepatic Cholangiocarcinoma	US	Taiho Oncology, Inc.	30 Sep 2022

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Biliary Tract Neoplasms	NDA/BLA	JP	Taiho Pharmaceutical Co., Ltd.	30 Jan 2022
Cholangiocarcinoma	Phase 3	JP	Taiho Pharmaceutical Co., Ltd.	29 Apr 2021
Adenocarcinoma of Esophagus	Phase 2	US	Taiho Oncology, Inc.	13 Jul 2023
Adenocarcinoma of Esophagus	Phase 2	FR	Taiho Oncology, Inc.	13 Jul 2023
Adenocarcinoma of Esophagus	Phase 2	DE	Taiho Oncology, Inc.	13 Jul 2023
Adenocarcinoma of Esophagus	Phase 2	ES	Taiho Oncology, Inc.	13 Jul 2023
Esophageal Squamous Cell Carcinoma	Phase 2	US	Taiho Oncology, Inc.	13 Jul 2023
Esophageal Squamous Cell Carcinoma	Phase 2	FR	Taiho Oncology, Inc.	13 Jul 2023
Esophageal Squamous Cell Carcinoma	Phase 2	DE	Taiho Oncology, Inc.	13 Jul 2023
Esophageal Squamous Cell Carcinoma	Phase 2	ES	Taiho Oncology, Inc.	13 Jul 2023

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04024436 (FOENIX-MBC2, SABCS2023)	Phase 2	Locally advanced breast cancer FGFR1 gene amplification	22	Futibatinib	hkcyrgqpbd(gtjxwdjvns) = 54.5% rfszioxkzo (cngqwawwca ) View more	Positive	05 Dec 2023
NCT04024436 (FOENIX-MBC2, SABCS2023)	Phase 2	Triple Negative Breast Cancer FGFR2 gene amplification	21	Futibatinib 20 mg	ggytkiuddd(gzktxtdhrd) = vaznevgqlc mawzevtsym (ukszofmsve, 1.2 - 30.4) View more	-	05 Dec 2023
JPRN-jRCT2080224975 (ESMO2023) Manual	Phase 1	Esophageal Carcinoma	92	Futibatinib + pembrolizumab (ICI naïve)	qdcfxiyrmg(lradejdeys) = lcsrzeuewk inuvwrckld (wuohsfjhyx ) View more	Positive	23 Oct 2023
JPRN-jRCT2080224975 (ESMO2023) Manual	Phase 1	Esophageal Carcinoma	92	Futibatinib + pembrolizumab (ICI refractory)	qdcfxiyrmg(lradejdeys) = bkpbvichgm inuvwrckld (wuohsfjhyx ) View more	Positive	23 Oct 2023
TAS-120-101 (EMA) Manual	Not Applicable	FGFR2 fusion or rearranged Cholangiocarcinoma	103	futibatinib	ylcvmkcxoq(rpxghiagkm) = ragxssjeey qvnssbwjhm (ztowrktbpb, 32 - 52) View more	Positive	18 Jul 2023
NCT02052778 (FOENIX-CCA2, ESMO_GI2023)	Phase 2	FGFR2 positive Intrahepatic Cholangiocarcinoma FGFR2	103	Futibatinib	zpcjqctlze(kilbgcfvtw) = zgfmrzigjd puujsfiynu (hkkmcgwukw ) View more	Positive	01 Jul 2023
NCT04189445 (SO-10, ESMO_GI2023)	Phase 2	FGFR2 positive Gastrooesophageal Junction Cancer FGFR2 amplification	28	Futibatinib 20 mg	qnlqtevvuk(vxcwuymmdo) = cfsgtrsphv bgmsvgyuid (affvydkahg, 6.1 - 36.9) View more	Positive	01 Jul 2023
TiFFANY (ASCO2023)	Phase 2	FGFR mutation-related tumors	26	Futibatinib 20 mg	ibasalnlyn(xugaiwvfll) = xnmgjvluwy bbwdogowij (kztvdzlgxp, 6.6–39.4) View more	Positive	31 May 2023
AACR2023 Manual	Phase 1	-	38	futibatinib (mild HI)	ortblqkfnl(wejtebctik) = iwnlrewnqt sdruwfomke (sbtfztfmoa ) View more	Positive	14 Apr 2023
AACR2023 Manual	Phase 1	-	38	futibatinib (moderate HI)	ortblqkfnl(wejtebctik) = glrjfvldws sdruwfomke (sbtfztfmoa ) View more	Positive	14 Apr 2023
NCT02052778 (FOENIX-CCA2, Pubmed \| Br Dent J)	Phase 2	Cholangiocarcinoma \| FGFR mutation-related tumors \| HR-positive/HER2-low Solid Tumors ... View more	103	Futibatinib 20 mg	sspfcicxey(slwxltqmjp) = yotmswbywb brurslafgl (youvagizvm ) View more	Positive	19 Jan 2023
JPRN-JapicCTI-195063 (ESMO2022)	Phase 1	Metastatic Solid Tumor \| Esophageal Carcinoma	-	Futibatinib 20 mg + Pembrolizumab 200 mg	hpcviqelzc(pbjwtclteq) = qxgocxukxb efaqawjsvb (fjhxommoek ) View more	-	10 Sep 2022

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