Advanced cervical cancer patients treated with standard of care (SOC) chemoradiation plus glutaminase inhibition with telaglenastat (CB-839) will have increased progression-free survival (PFS) compared to historical rates for patients receiving SOC chemoradiation alone.

Start Date31 Dec 2025

Sponsor / Collaborator

Washington University School of Medicine

[+2]

NCT04824937

/ Unknown statusPhase 2IIT

A Phase II Study of the Glutaminase Inhibitor Telaglenastat (CB-839) in Combination With the PARP Inhibitor Talazoparib in Participants With Metastatic Castration-Resistant Prostate Cancer

The purpose of this research is to test the effectiveness of an experimental drug combination for people with metastatic castration-resistant prostate cancer (mCRPC).
The names of the study drugs involved in this study are:
* Telaglenastat (CB-839)
* Talazoparib

Start Date01 Jul 2021

Sponsor / Collaborator

The General Hospital Corp.

[+3]

NCT04250545

/ Active, not recruitingPhase 1IIT

A Phase 1 Trial of MLN0128 (Sapanisertib) and CB-839 HCl (Telaglenastat) in Advanced NSCLC Patients

This phase I/Ib trial studies the side effects and best dose of CB-839 HCl when given together with sapanisertib in treating patients with non-small cell lung cancer that has spread to other places in the body (advanced). CB-839 HCl and sapanisertib may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth.

Start Date26 Oct 2020

Sponsor / Collaborator

National Cancer Institute

100 Clinical Results associated with Telaglenastat

100 Translational Medicine associated with Telaglenastat

100 Patents (Medical) associated with Telaglenastat

306

Literatures (Medical) associated with Telaglenastat

01 Jul 2025·BIOORGANIC CHEMISTRY

Deciphering the landscape of allosteric glutaminase 1 inhibitors as anticancer agents

Review

Author: Fossa, Paola ; Carbone, Anna ; Trombetti, Gabriele ; Orro, Alessandro ; Francesconi, Valeria ; D'Ursi, Pasqualina ; Tonelli, Michele ; Dreassi, Elena ; Schenone, Silvia ; Vagaggini, Chiara ; Poggialini, Federica

Glutamine is the second most utilised energy source after glucose for cancer cells to support their proliferation and survival. Glutaminase 1 (GLS1) is the rate-limiting enzyme during the glutaminolysis pathway and thus represents a promising therapeutic target for the development of innovative antitumor agents. Two main classes of GLS1 inhibitors, based on their different binding mode, are reported: the substrate active site and the allosteric site inhibitors. Despite the intense efforts made to date, only two GLS1 inhibitors (i.e.,CB-839 and IPN60090) have entered clinical trials. Therefore, this research field remains to be explored to improve the effectiveness of anticancer therapy. Hence, we describe the discovery and development of reversible allosteric GLS1 inhibitors disclosed in the last six years, dividing them based on their structural similarity with bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide (BPTES) and CB-839. Furthermore, macrocyclic and thiadiazole derivatives, and other structurally different compounds are discussed to present a wider picture of the chemical space under investigation. The study of the binding interactions governing GLS1 inhibition is also analyzed, to help prospectively refine the structural features for greater efficacy. Interestingly, an overview of a new class of irreversible allosteric inhibitors targeting GLS1 Lys320 key residue is provided for the first time. We also summarize the most important biological studies conducted on CB-839 and IPN60090 and their significance for further assessment. The insights garnered from this paper are expected to guide future drug design endeavours toward the identification of novel therapeutics targeting GLS1 to complement and potentially enhance the arsenal of anticancer medications.

01 Jul 2025·Science China-Life Sciences

Glutaminolysis and α-ketoglutarate-stimulated KCa3.1 expression contribute to β-adrenoceptor activation-induced myocardial fibrosis in mice

Article

Author: Zhang, Yi ; Deng, Xiu-Ling ; Guo, Chen ; Wu, Lin-Hong ; Han, Meng-Zhuan ; She, Gang ; Yang, Yi-Yi ; Du, Xiao-Jun ; Li, Jing-Jing ; Zhao, Li-Mei ; Pang, Zheng-Da ; Wang, Yan ; Zhao, Xin-Yi ; Bai, Ru-Yue ; Jiao, Lian-Ying ; Hai, Xia-Xia

Heart failure is associated with myocardial fibrosis, a pivotal histopathological feature arising from β-adrenergic receptor (β-AR) stimulation through sympathetic nervous system activation. Augmented glutaminolysis with increased bioavailability of α-ketoglutarate (α-KG) is suggested to contribute to fibrogenesis and changes in cellular gene expression. K_Ca3.1 is a calcium-activated potassium channel expressed in fibroblasts and has been implicated in mediating fibrosis, yet the putative interactions between glutaminolysis and K_Ca3.1 in β-AR-mediated cardiac fibrosis remain poorly understood. Here, we performed a series of in vitro and in vivo experiments to investigate how α-KG might influence the expression of K_Ca3.1 in the context of experimental myocardial fibrosis driven by β-AR activation. In cultured adult mouse cardiac fibroblasts, α-KG exposure resulted in the upregulation of K_Ca3.1 mRNA and protein levels that were commensurate with the dose and duration of exposure, and also led to increased K_Ca3.1 channel currents. Exposure to α-KG led to a significant decrease in levels of histone methylation (H3K27me3) within the K_Ca3.1 promoter, a decrease in the association of the transcription repressor REST from this site, as well as an enrichment of transcription activator AP-1 binding. The exacerbated fibrotic signaling induced by α-KG in cultured fibroblasts was suppressed by functional inhibition of K_Ca3.1 or by genetic knockdown of Kcnn4. Moreover, β-AR activation by isoproterenol significantly augmented glutaminolysis mediated by glutaminase 1 (GLS1) and significantly increased α-KG levels detected in the supernatant of cultured fibroblasts and cardiomyocytes. In addition, isoproterenol-induced K_Ca3.1 expression in fibroblasts was curtailed by treatment with the GLS1 inhibitor CB-839, or by GLS1 gene knockdown, or by treatment with the selective β₂-AR antagonist, ICI118551. In mouse models of established cardiac fibrosis evoked by isoproterenol-stimulation or β₂-AR overexpression, treatment with CB-839 for 4 weeks suppressed the phenotypic features of fibrosis, and this was associated with a decline in α-KG tissue content, a lack of histone demethylation at the K_Ca3.1 promoter, as well as suppression of K_Ca3.1 expression. Taken together, our study demonstrates for the first time that glutaminolysis contributes to β-AR activation-induced myocardial fibrosis via α-KG-stimulated K_Ca3.1 expression. We anticipate that treatments which target the β-AR/GLS1/α-KG/K_Ca3.1 signaling pathway might be effective for cardiac fibrosis.

23 Jun 2025·CELLULAR AND MOLECULAR LIFE SCIENCES

The metabolic shift of glutaminase 2 to glutaminase 1 promotes LGR5 + progenitor cell proliferation in liver cirrhosis.

Article

Author: de Meijer, Vincent E ; He, Kang ; Kong, Defu ; Blokzijl, Hans ; Heegsma, Janette ; Faber, Klaas Nico ; Zhou, Qi

BACKGROUND AND AIM:

Liver regeneration is impaired in end-stage liver disease characterized by advanced fibrosis and cirrhosis, where metabolic reprogramming is considered as a therapeutic target. The shift in glutaminolysis from liver-type Glutaminase 2 (GLS2) to kidney-type Glutaminase 1 (GLS1) is crucial in different liver diseases, though its role in liver progenitor cell-mediated regeneration remains unclear. This study aimed to analyze the expression of glutamine-metabolizing enzymes in fibrotic human livers and investigate the role of GLS1 in LGR5⁺-progenitor cell expansion in liver regeneration.

METHODS:

Healthy and chronically diseased human liver tissue from patients with alcoholic liver disease, viral hepatitis, biliary atresia, primary biliary cholangitis or non-alcoholic steatohepatitis were immunostained for GLS1, GLS2 and glutamine synthetase (GS), and co-stained for LGR5. GLS1 was inhibited in adult progenitor cell-rived human liver organoids to evaluate its role in stemness and cell proliferation pathways.

RESULTS:

GLS1 expression was enhanced and GLS2 decreased in chronic liver diseases compared to healthy liver. GLS1 was expressed in parenchymal, including hepatocytes, and non-parenchymal cells. In cirrhotic livers, GLS1⁺ hepatocytes showed a spatial distribution comparable to the progenitor cell marker LGR5. The GLS1 inhibitor CB839 suppressed progenitor cell markers (LGR5 and AXIN2) via the ROS-Wnt/β-Catenin pathway, which was rescued by glutathione (GSH). The CB839-mediated decrease in cell proliferation in human liver organoids was rescued by non-essential amino acids.

CONCLUSIONS:

This study identifies GLS1 as a metabolic regulator of progenitor cell expansion aiding liver regeneration in various etiologies of human liver cirrhosis.

News (Medical) associated with Telaglenastat

01 May 2025

·www.prnewswire.com

Synhale Therapeutics Acquires Telaglenastat, Accelerates Development for Pulmonary Hypertension Treatment

PITTSBURGH and BOSTON, May 1, 2025 /PRNewswire/ -- Synhale Therapeutics Inc. (Synhale), a virtual, clinical-stage biotech company committed to transforming Pulmonary Hypertension (PH), announced the acquisition of Telaglenastat (CB-839), the first-in-class glutaminase inhibitor. Synhale is advancing into a Phase 2 clinical program across PH Groups 1-4. "This acquisition represents a unique opportunity to rapidly deliver clinical data addressing a disease with high mortality and substantial market potential," said Chad D. Holland, President & CEO of Synhale. "Leveraging Telaglenastat's prior human clinical experience, our capital-efficient model aims to accelerate transformative therapy to patients while maximizing shareholder value." Stephen Chan, MD, PhD, Founder of Synhale, added, "The unmet patient need in PH is immense, particularly in Groups 2 and 3, where heart failure with preserved ejection fraction (HFpEF) and chronic lung disease remain deadly and underserved. PH with HFpEF carriers a five-year mortality approaching 50%, with similarly grim outcomes in COPD and other lung diseases. By targeting glutaminase activity, we address a fundamental metabolic pathway across all PH groups, offering hope to patients with few options." PH, a severe condition, is characterized by remodeling and stiffening in the pulmonary vasculature and often dramatically increases mortality risk when combined with other conditions. Current classifications fail to reflect the molecular drivers of PH, leaving treatment gaps. Synhale's approach with Telaglenastat targets elevated glutaminase activity, a key driver of vascular, cardiac, and pulmonary pathology, potentially benefiting not only rare Pulmonary Arterial Hypertension (Group 1) and chronic thromboembolic disease (Group 4) but also more prevalent PH linked to heart failure (Group 2) and chronic lung disease (Group 3). Telaglenastat, previously dosed in over 800 patients during oncology development, is Phase 2-ready with extensive preclinical data for PH. Synhale's clinical advancement strategy addresses an estimated $12B-$24B market opportunity across PH Groups 1-4. "We are embarking on our next round of fundraising to advance Telaglenastat through critical clinical milestones," added Holland. "Our virtual operating model enables us to be capital-efficient while maintaining world-class expertise focused on delivering breakthrough therapies for PH patients." About Synhale Therapeutics Synhale Therapeutics Inc. is a virtual biotech company dedicated to transforming Pulmonary Hypertension treatment by targeting elevated glutaminase activity—a key driver of vascular stiffness, fibrosis, and proliferation. Synhale's mission is to redefine PH treatment through mechanism-driven therapies that address the root cause of this disease. For Media & Investor Inquiries: Chad D. Holland [email protected] 617-758-8643 SOURCE Synhale Therapeutics Inc. WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

AcquisitionPhase 2

10 Jan 2023

·www.fiercebiotech.com

Cash-strapped Calithera closes down in shadow of enrollment delays to cancer trials

"We truly wish the outcome was different today,” Calithera Biosciences CEO Susan Molineaux, Ph.D., said in a release. Calithera Biosciences has kept its head down since a phase 2 fail in 2021 caused layoffs for a third of its workforce. But in the wake of enrollment delays for two lead cancer therapies, the cash-strapped biotech has given up the fight and announced it’s liquidating the business. “The board of directors and management devoted substantial time and effort in identifying and pursuing various opportunities, but we were unable to complete a transaction that would allow us to continue the development of our clinical programs and enhance shareholder value,” CEO Susan Molineaux, Ph.D., said in a release Monday. As a result, all clinical programs will be shut down, with “most” of the company’s employees terminated by the end of this quarter. “Importantly, I would like to sincerely thank our employees and others who have supported Calithera over the years,” Molineaux added in her statement yesterday. “We appreciate your partnership and participation, and we truly wish the outcome was different today.” Money had been tight at the biotech for a while. Calithera had cash and equivalents of $34.1 million at the end of September, which was only expected to last into the second quarter of this year. In November, the company revealed it was “evaluating all options for its programs, including strategic collaboration or licensing agreements and actively considering the sale of certain programs, in order to extend its cash runway.” It can’t have helped that things weren’t quite going to plan for its lead programs, either. Calithera also used its November financial report to reveal that “site activation delays” meant that enrollment for trials of sapanisertib and mivavotinib had been “slower than anticipated.” Still, the company said at the time that initial data from these studies were expected in mid-2023, with sapanisertib having secured an FDA fast-track tag for non-small cell lung cancer in October. The biotech licensed both drugs from Takeda in 2021 after the failure of its own drug telaglenastat in a midstage kidney cancer test prompted Calithera to wield the ax on 35% of staff. Calithera's announcement is just the latest in a string of recent closures for struggling biotechs, with Otonomy winding down in December, followed by Nabriva Therapeutics last week.

Fast TrackFinancial Statement

14 Nov 2022

·www.globenewswire.com

Calithera Biosciences Reports Third Quarter 2022 Financial Results and Business Update

-- Conference Call and Webcast Scheduled for 5:00 p.m. ET on Monday, November 14, 2022 --SOUTH SAN FRANCISCO, Calif., Nov. 14, 2022 (GLOBE NEWSWIRE) -- Calithera Biosciences, Inc. (Nasdaq: CALA), a clinical-stage, precision-oncology biopharmaceutical company, today announced its financial results for the third quarter ended September 30, 2022. “Earlier in the fourth quarter, we were very pleased to announce that we received FDA Fast Track designation for sapanisertib. This designation facilitates more frequent communication with the Agency, as well as a number of other benefits that could support our efforts to bring sapanisertib to patients in this area of high unmet need more quickly,” said Susan Molineaux, PhD, president and chief executive officer of Calithera. “Today we also share that we have experienced site activation delays on both our sapanisertib and mivavotinib trials, leading to slower than anticipated enrollment for both these programs. We expect initial data from these studies will not be available until mid-2023.” Third Quarter 2022 and Other Recent Highlights Received FDA Fast Track designation for sapanisertib (dual mTORC 1/2 inhibitor). In October, Calithera announced that sapanisertib has been granted Fast Track designation by the FDA for the treatment of adult patients with unresectable or metastatic squamous non-small cell lung cancer (sqNSCLC) whose tumors harbor the NRF2 mutation. Fast Track designation, which is designed to facilitate the development and expedite the review of therapeutic candidates with the potential to treat a serious or life-threatening condition where there is a major unmet medical need, provides a number of potential benefits including increased communication with the FDA, the ability to submit a marketing application on a rolling basis and the possibility of priority review. Began enrolling patients in Phase 2 trial evaluating sapanisertib in sqNSCLC. In July 2022, the Company began enrolling patients in its phase 2 clinical trial (NCT05275673) of the dual mTORC 1/2 inhibitor sapanisertib (CB-228) in patients with relapsed/refractory NRF2 (NFE2L2)-mutated sqNSCLC. The study is designed to confirm the selective activity of sapanisertib in NRF2-mutated tumors compared to wild-type tumors, and to refine dose in this biomarker-defined population. The primary endpoints of the study are investigator-assessed overall response rate (ORR) per RECIST v1.1, and safety. Calithera presented a trial-in-progress poster detailing the study design at the North American Conference on Lung Cancer in September 2022. Continued patient enrollment activities in Phase 2 trial evaluating mivavotinib (SYK inhibitor) in r/r non-GCB DLBCL. In June 2022, the Company began enrolling patients in its multicenter Phase 2 clinical trial (NCT05319028) evaluating mivavotinib (CB-659) in patients with relapsed/refractory non-germinal center B-cell like (non-GCB) diffuse large B-cell lymphoma (DLBCL). The main objectives of the study are to confirm previously observed single-agent activity in non-GCB DLBCL patients, evaluate activity according to MYD88/CD79b mutation status and refine dose/schedule in this patient population. The primary endpoints of the study are overall response rate (as assessed by an independent radiology review committee) and safety. Details of the Phase 2 study design were presented in a trial-in-progress poster at the Pan Pacific Lymphoma Conference in July. Continued to advance VPS4 program through lead optimization. Calithera continued to advance multiple vacuolar protein sorting-associated protein 4A (VPS4A) and VPS4B inhibitors through lead optimization and plans to share updates on this program by the end of 2022. Selected Third Quarter 2022 Financial Results Cash and cash equivalents totaled $34.1 million at September 30, 2022. Based on its current operating plan, the Company expects it has sufficient cash to fund its operations into the second quarter of 2023. The Company is currently evaluating all options for its programs, including strategic collaboration or licensing agreements and actively considering the sale of certain programs, in order to extend its cash runway. Research and development expenses for the third quarter 2022 were $6.5 million, compared to $11.6 million in the same period prior year. The decrease of $5.1 million was primarily due to decreases in the telaglenastat and CB-280 programs and investments in early stage research, partially offset by increases in the sapanisertib and mivavotinib programs. General and administrative expenses for the third quarter 2022 were $3.0 million, compared to $6.3 million in the same period prior year. The decrease of $3.3 million was primarily due to decreased personnel-related costs and legal expenses. Net loss was $9.8 million for the three months ended September 30, 2022. Conference Call Information Calithera will host an update conference call today, Monday, November 14, at 2:00 p.m. Pacific Time/5:00 p.m. Eastern Time. To register for dial-in access to the call, please use this link. To access the live audio webcast or the subsequent archived recording, visit the Investors section of the Calithera website at www.calithera.com. The webcast will be recorded and available for replay on Calithera’s website for 30 days. About Calithera Calithera Biosciences is a clinical-stage, precision oncology biopharmaceutical company developing targeted therapies to redefine treatment for biomarker-specific patient populations. Driven by a commitment to rigorous science and a passion for improving the lives of people impacted by cancer, Calithera is advancing a robust pipeline of investigational, small-molecule oncology compounds with a biomarker-driven approach that targets genetic vulnerabilities in cancer cells to deliver new therapies for patients suffering from aggressive hematologic and solid tumor cancers for which there are currently limited treatment options. Calithera is headquartered in South San Francisco, California. For more information about Calithera, please visit www.calithera.com. Forward Looking Statements Statements contained in this press release regarding matters that are not historical facts are "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995. Words such as "may," "will," "expect," "anticipate," "estimate," "intend," "poised" and similar expressions (as well as other words or expressions referencing future events, conditions, or circumstances) are intended to identify forward-looking statements. These statements include those related to the safety, tolerability and efficacy of Calithera’s product candidates, the overall advancement of Calithera’s product candidates in preclinical development and clinical trials, including the availability of initial data for the mivavotinib and sapanisertib trials by mid-2023, Calithera’s ability to potentially initiate registrational studies in biomarker-specific populations in DLBC and relapsed or refractory squamous NSCLC, the expectation that VPS4 inhibitors will be well-tolerated and have strong single-agent activity in tumors with certain mutations, Calithera’s plan to advance multiple VPS4 series through lead optimization and plan to share updates on this program by the end of the year, the unmet need in the treatment of patients with advanced disease, Calithera’s expectation that cash and cash equivalents will be sufficient to meet its current operating plan into the second quarter of 2023 and whether Calithera will be able to enter into strategic collaborations or licensing agreements or sell certain programs and sufficiently extend its cash runway. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements. The potential product candidates that Calithera develops may not progress through clinical development or receive required regulatory approvals within expected timelines or at all. In addition, clinical trials may not confirm any safety, potency or other product characteristics described or assumed in this press release. Such product candidates may not be beneficial to patients or be successfully commercialized. The failure to meet expectations with respect to any of the foregoing matters may have a negative effect on Calithera's stock price. Additional information concerning these and other risk factors affecting Calithera's business can be found in Calithera's periodic filings with the Securities and Exchange Commission at www.sec.gov. These forward-looking statements are not guarantees of future performance and speak only as of the date hereof, and, except as required by law, Calithera disclaims any obligation to update these forward-looking statements to reflect future events or circumstances. Calithera Biosciences, Inc. Selected Consolidated Statements of Operations Financial Data(in thousands) (unaudited) Three Months EndedSeptember 30, Nine Months EndedSeptember 30, 2022 2021 2022 2021Revenue: License revenue $— $6,750 $— $9,750 Total revenue — 6,750 — 9,750 Operating expenses: Research and development 6,447 11,556 23,771 39,715 General and administrative 3,079 6,344 10,957 16,259 Total operating expenses 9,526 17,900 34,728 55,974 Loss from operations (9,526) (11,150) (34,728) (46,224)Other income (expense): Transaction costs allocable to warrant liabilities — — (475) — Change in fair value of warrants liabilities (453) — 2,253 — Interest and other income (expense), net 177 (22) 236 346 Other income (expense), net (276) (22) 2,014 346 Net loss $(9,802) $(11,172) $(32,714) $(45,878) Calithera Biosciences, Inc. Selected Consolidated Balance Sheet Financial Data (in thousands) (unaudited) September 30, December 31, 2022 2021Balance Sheet Data: Cash and cash equivalents$34,068 $59,537 Working capital 25,465 47,446 Total assets 37,083 64,756 Total liabilities 10,695 15,672 Convertible preferred stock 22,342 40,702 Accumulated deficit (505,680) (491,326)Total stockholders’ equity 26,388 8,382 CONTACTS:Stephanie Wong ir@Calithera.com 650.870.1063 INVESTORS:Burns McClellanLee Roth212.213.0006lroth@burnsmc.com MEDIA:Sam Brown, Inc.Hannah Hurdle805.338.4752hannahhurdle@sambrown.com

Phase 2Financial StatementFast TrackPhase 1

100 Deals associated with Telaglenastat

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KEGG	Wiki	ATC	Drug Bank
D11738	-	-	DB15232

R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Advanced Cervical Carcinoma	Phase 2	United States	Calithera Biosciences, Inc.	31 Dec 2025
Metastatic castration-resistant prostate cancer	Phase 2	United States	Calithera Biosciences, Inc.	01 Jul 2021
Metastatic castration-resistant prostate cancer	Phase 2	United States	Pfizer Inc.	01 Jul 2021
Non-squamous non-small cell lung cancer	Phase 2	United States	Calithera Biosciences, Inc.	24 Jul 2020
Advanced Lung Non-Small Cell Carcinoma	Phase 2	United States	National Cancer Institute	16 Mar 2020
EGFR-mutated non-small Cell Lung Cancer	Phase 2	United States	National Cancer Institute	16 Mar 2020
metastatic non-small cell lung cancer	Phase 2	United States	National Cancer Institute	16 Mar 2020
Neurofibrosarcoma	Phase 2	United States	National Cancer Institute	14 Dec 2019
Unresectable Solid Neoplasm	Phase 2	United States	National Cancer Institute	14 Dec 2019
KRAS mutant Colorectal Cancer	Phase 2	United States	Calithera Biosciences, Inc.	25 Jun 2019

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT03831932 (CTgov)	Phase 1/2	Advanced Lung Non-Small Cell Carcinoma \| metastatic non-small cell lung cancer \| EGFR-mutated non-small Cell Lung Cancer	23	telaglenastat hydrochloride+Osimertinib (Phase 1b Cohorts)	nzzfkzdbiq = mwkibepozr uxqsnrgpfd (rdjhrxkzdi, pgixldyhpn - yjmvryoqkb) View more	-	19 Jun 2025
				Telaglenastat HCl (Phase 1b 400mg Telaglenastat HCl Cohort)	ugpvthlrdr(klzipljaop) = vmzhamlxkc uhennxgvwm (gnkqdnyuuh, nhsxuihcya - avuypyihvy) View more
NCT02861300 (CTgov)	Phase 1/2	Rectal Cancer \| RAS mutant Colorectal Cancer \| Colonic Cancer ... View more	50	CB-839+capecitabine (Phase I)	megcyxduxl = dvujdmzdqy umrgyhvavb (qulvdghyix, rejewwtnxe - qlxnxbkvtm)	-	19 Dec 2024
				CB-839+Capecitabine (Phase I Dose -1)	rifeqwmctn = tvzgxrrttn moifkccauu (fzvrwrzcid, raelrkpmnm - lxqraapipk) View more
NCT03047993 (Pubmed \| Nat Cancer) Manual	Phase 1/2	Myelodysplastic Syndromes glutamine transporter solute carrier family 38 member 1	30	Telaglenastat (CB-839) + Azacytidine (AZA)	ilpuyufbrb(lvaojjcpvw) = kitlrqztoh fzycjetrez (kzopanjzeo ) View more	Positive	19 Sep 2024
NCT03263429 (P-187, CTgov)	Phase 1/2	Refractory Colorectal Carcinoma \| Metastatic Colorectal Carcinoma \| RAS Wild Type Colorectal Cancer	29	Pharmacological Study+Glutaminase Inhibitor CB-839+Irinotecan Hydrochloride (phase I only)+Panitumumab	igrgfomdal = nyzvxqnziz ptrwlsyudk (mupirwftgp, taeuhpxxgq - oqxkrbzujl) View more	-	30 Aug 2024
NCT03047993 (CTgov)	Phase 1/2	High Risk Myelodysplastic Syndrome \| Acute myeloid leukemia with multilineage dysplasia \| Chronic Myelomonocytic Leukemia	28	Glutaminase Inhibitor CB-839+Azacitidine	rroentkuep = hvnydkldev vwnttorlhh (ebqfjwmcnb, pihnmtwogm - volxbnyacs) View more	-	14 May 2024
NCT03428217 (CANTATA, CTgov)	Phase 2	Metastatic Renal Cell Carcinoma \| Advanced Renal Cell Carcinoma \| Metastatic Clear Cell Renal Cell Carcinoma	444	Placebo+Cabozantinib (Pbo-Cabo)	ojjppyygpj(dfqmtaimib) = fdbshfwqum ccfajvawbt (akglddovbq, wvgqokkcsl - rsbkexrgwj) View more	-	20 Mar 2023
				CB-839+Cabozantinib (CB-Cabo)	ojjppyygpj(dfqmtaimib) = rsyzqslogf ccfajvawbt (akglddovbq, qbsgavkxee - tyjyufzfdn) View more
NCT02771626 (O16, CTgov)	Phase 1/2	Renal Cell Carcinoma \| Non-Small Cell Lung Cancer \| Metastatic melanoma ... View more	118	Nivolumab+CB-839 (Telaglenastat 600 mg + Standard Dose Nivolumab)	ltbtehbcnb = najxziazyr nenykvvtyy (ximforqjyd, yrvvzbwqli - jhowoaoyxk) View more	-	17 Mar 2023
				Nivolumab+CB-839 (Telaglenastat 800 mg + Standard Dose Nivolumab: ccRCC Naïve to Checkpoint Inhibitors)	ltbtehbcnb = uhljrllilu nenykvvtyy (ximforqjyd, gixgkfmyzo - asglmfifab) View more
NCT03798678 (ASH 12022 \| ASH 22022) Manual	Phase 1	Relapse multiple myeloma	21	Dexamethasone+Carfilzomib+Telaglenastat	eefrlipflf(dknmzvlvwg) = smxxuiqiah pfxhemyoaz (joocfbxuib ) View more	Positive	15 Nov 2022
NCT03057600 (P6-20-07, CTgov)	Phase 2	Advanced Triple-Negative Breast Carcinoma	52	CB-839+Paclitaxel (Cohort 1 - African Ancestry, 3rd Line+)	kigvzyylqc = siquqmuhik dwofeftxyf (bcviluaqgx, chbluetsxl - loydsyostv) View more	-	28 Sep 2022
				CB-839+Paclitaxel (Cohort 2 - African Ancestry, 1st Line)	kigvzyylqc = fcspfpyqsw dwofeftxyf (bcviluaqgx, bzpxwobuzh - vhxjkytdna) View more
NCT03163667 (ENTRATA, CTgov)	Phase 2	Metastatic Clear Cell Renal Cell Carcinoma	69	Placebo+everolimus (Placebo + Everolimus)	afpwtujyoi(vsvbfjhtym) = xadsosismk ojrxdzixnz (fpzpxbjcdz, wsdvrnylvj - bvxpzmgjxv) View more	-	15 Sep 2022
				CB-839+everolimus (CB-839 + Everolimus)	afpwtujyoi(vsvbfjhtym) = rkhkmpprni ojrxdzixnz (fpzpxbjcdz, rjmhknawvy - jxflzjwvjz) View more

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