RegulationFast Track (United States), Accelerated Approval (United States), Orphan Drug (United States), Breakthrough Therapy (China), Orphan Drug (South Korea), Orphan Drug (Australia), Conditional marketing approval (United States), Priority Review (United States), Breakthrough Therapy (United States)

Structure/Sequence

Molecular FormulaC30H30F2N6O3

InChIKeyNXQKSXLFSAEQCZ-UHFFFAOYSA-N

CAS Registry2296729-00-3

Clinical Trials associated with Sotorasib

NCT06892054

/ Not yet recruitingPhase 2IIT

Sotorasib Combined with First-line Chemotherapy for Advanced Pancreatic Adenocarcinoma with KRAS P.G12C Mutation

The main objective of this trial is to evaluate the safety and tolerability of sotorasib combined with first-line chemotherapy for advanced pancreatic adenocarcinoma harboring KRAS p.G12C mutation.

Start Date30 Jun 2025

Sponsor / Collaborator

Groupe Coopérateur Multidisciplinaire en Oncologie

[+1]

NCT06068153

/ WithdrawnPhase 2IIT

A Multicentre, Single-arm Phase II Trial of Sotorasib Plus Lenvatinib, As Second-line Treatment in Patients with KRASG12C-mutant, Metastatic NSCLC

AMBER is a multicentre, single-arm phase II trial. The protocol treatment consists of of sotorasib plus lenvatinib, as a second-line treatment. The primary objective of the trial is to evaluate the clinical efficacy of sotorasib plus lenvatinib, in terms of objective response rate, for patients with KRASG12C-mutant, metastatic NSCLC.

Start Date01 Mar 2025

Sponsor / Collaborator

Amgen, Inc.

[+1]

NCT06804824

/ RecruitingPhase 1

A Phase 1/1b, Open-Label, Multicenter, First-in-Human Dose Escalation and Dose Expansion Study to Evaluate the Safety, Tolerability, Pharmacokinetics, Pharmacodynamics, and Anti-Tumor Activity of VVD-159642, a RAS-PI3Kα Inhibitor, as a Single Agent and in Combination in Participants With Advanced Solid Tumors

A FIH study to evaluate the safety, tolerability, pharmacokinetics (PK), pharmacodynamics (PD), and preliminary anti-tumor activity of VVD-159642, a rat sarcoma viral oncogene-phosphatidylinositol 3-kinase alpha (RAS-PI3Kα) inhibitor, as a single agent and in combination with either sotorasib or trametinib in participants with advanced solid tumors.

Start Date25 Feb 2025

Sponsor / Collaborator

Vividion Therapeutics, Inc.

100 Clinical Results associated with Sotorasib

100 Translational Medicine associated with Sotorasib

100 Patents (Medical) associated with Sotorasib

610

Literatures (Medical) associated with Sotorasib

01 Dec 2025·CANCER CHEMOTHERAPY AND PHARMACOLOGY

Evolution of computational techniques against various KRAS mutants in search for therapeutic drugs: a review article

Review

Author: Subramaniyan, Vetriselvan ; Ogaly, Hanan A ; Mehmood, Ayesha ; Khalid, Asaad ; Wadood, Abdul ; Hakami, Mohammed Ageeli

KRAS was (Kirsten rat sarcoma viral oncogene homolog) revealed as an important target in current therapeutic cancer research because alteration of RAS (rat sarcoma viral oncogene homolog) protein has a critical role in malignant modification, tumor angiogenesis, and metastasis. For cancer treatment, designing competitive inhibitors for this attractive target was difficult. Nevertheless, computational investigations of the protein's dynamic behavior displayed the existence of temporary pockets that could be used to design allosteric inhibitors. The last decade witnessed intensive efforts to discover KRAS inhibitors. In 2021, the first KRAS G12C covalent inhibitor, AMG 510, received FDA (Food and drug administration) approval as an anticancer medication that paved the path for future treatment strategies against this target. Computer-aided drug designing discovery has long been used in drug development research targeting different KRAS mutants. In this review, the major breakthroughs in computational methods adapted to discover novel compounds for different mutations have been discussed. Undoubtedly, virtual screening and molecular dynamic (MD) simulation and molecular docking are the most considered approach, producing hits that can be employed in subsequent refinements. After comprehensive analysis, Afatinib and Quercetin were computationally identified as hits in different publications. Several authors conducted covalent docking studies with acryl amide warheads groups containing inhibitors. Future studies are needed to demonstrate their true potential. In-depth studies focusing on various allosteric pockets demonstrate that the switch I/II pocket is a suitable site for drug designing. In addition, machine learning and deep learning based approaches provide new insights for developing anti-KRAS drugs. We believe that this review provides extensive information to researchers globally and encourages further development in this particular area of research.

01 Jun 2025·EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY

Design, synthesis, and antitumor activity of stapled peptide inhibitors targeting the RAS–RAF interactions

Article

Author: Gai, Conghao ; Zhang, Peichao ; Chai, Xiaoyun ; Yu, Zhou ; Zhu, Lie ; Zhang, Kai ; Zhao, Qingjie ; Zou, Yan ; Zhuo, Xiaobing ; Han, Dan

RAS-RAF interactions play a vital role in the RAS-RAF-MEK-ERK signaling pathway, significantly regulating cell proliferation, differentiation, and survival. Some small molecule inhibitors targeting various components of this pathway, such as MRTX849 and AMG 510, have been introduced for clinical application. However, peptide-based drugs encounter several challenges, such as poor cell permeability, low biological stability, and rapid in vivo clearance, which hinder their application. Herein, based on co-crystal complex structures and RAS-RAF interaction hotspots, we identified four linear peptides-Raf-0 to Raf-2 and CRD-0-derived from the α-helical regions of the RAS-binding domain (RBD) and the cysteine-rich domain (CRD) of CRAF. Raf-1 was selected for further modification using a hydrocarbon stapling strategy, capping it with stearic acid at the N-terminal due to its highest binding affinity in the SPR assay. As a result, Sraf-2-1 and Sraf-7-1 bound to KRAS^G12C with K_d values of 3.56 μM and 2.62 μM, respectively, demonstrating robust anticancer activity in the CCK8 assay. Additionally, Sraf-2-1 and Sraf-7-1 reduced AKT phosphorylation, induced cancer cell apoptosis in a concentration-dependent manner, and effectively inhibited cancer cell migration, showing improved α-helix stability and cell permeability. In summary, our findings indicate that the hydrocarbon stapling strategy and stearic acid tagging enhanced the therapeutic potential of peptide inhibitors, offering methods for targeting RAS in cancer therapy.

01 May 2025·PHARMACOLOGICAL RESEARCH

Targeting USP47 enhances the efficacy of KRAS inhibitor in KRASG12C mutated non-small cell lung cancer by controlling deubiquitination of c-Myc

Article

Author: Choo, Hyunah ; Shin, Sang Chul ; Hwang, Inah ; Shin, Hyungkyung ; Hwang, SuA ; Song, Eun Joo ; Kim, Jinhyeok ; Oh, Yeonji ; Jeong, Jeong Hyun ; Kim, Eunice EunKyeong

FDA-approved KRAS^G12C inhibitors, like Sotorasib, target G12C-mutated KRAS in NSCLC. However, issues with insensitivity and drug resistance have emerged, requiring the development of new combination therapies to overcome these limitations. USP47 has been identified as a regulator of cancer-related signaling pathways such as Wnt, Hippo, and p53. However, its role in the KRAS signaling pathway remains largely unexplored and USP47 inhibitors are less developed than those targeting its homolog, USP7. Here, we identify USP47 as a novel therapeutic target in KRAS^G12C-mutated NSCLC and report K-552, a selective USP47 inhibitor, as a potential treatment strategy. We demonstrate that USP47 stabilizes c-Myc by preventing its proteasomal degradation through deubiquitination, thereby promoting NSCLC cell proliferation. Additionally, the compound K-552, a USP47 inhibitor identified through virtual screening, effectively destabilizes c-Myc and inhibits KRAS^G12C-mutated NSCLC cell proliferation. Furthermore, USP47 inhibition-either by siRNA knockdown or K-552 treatment-enhances the efficacy of Sotorasib in vitro and in vivo. Together, our findings establish USP47 as a promising therapeutic target in KRAS^G12C-mutated NSCLC and introduce K-552 as a USP47 inhibitor with potential for combination therapy with KRAS^G12C inhibitors.

425

News (Medical) associated with Sotorasib

04 Apr 2025

·pipelinereview.com

Vividion Therapeutics Doses First Patient in Phase I Study of RAS-PI3Kα Inhibitor for Treatment of Advanced Solid Tumors

SAN DIEGO, CA, USA & BERLIN, Germany I April 03, 2025 I Vividion Therapeutics, Inc. (Vividion) today announced that the first patient has been dosed in a Phase I clinical trial evaluating VVD-159642, an investigational oral inhibitor designed to target RAS-driven cancers. Vividion is a clinical-stage biopharmaceutical company, and a wholly owned and independently operated subsidiary of Bayer AG, utilizing innovative discovery technologies to unlock targets with strong disease-link, yet traditionally undruggable and develop small molecule precision therapeutics for devastating cancers and immune disorders. The new Phase I study ( NCT06804824 ) will evaluate the safety, tolerability, pharmacokinetics, pharmacodynamics and preliminary anti-tumor activity of VVD-159642 as a single agent and in combination with either sotorasib or trametinib in patients with advanced solid tumors. “Despite being a major driver in approximately 20% of cancers, the RAS gene has proven exceptionally difficult to target with drugs, largely due to its essential role in the RAS-PI3Kα signaling pathway, which is vital for healthy cell function,” said Jenna Goldberg, M.D., Chief Medical Officer of Vividion. “VVD-159642 is designed and being studied to selectively prevent RAS activation of the PI3Kα pathway, thus blocking oncogenic signaling without disrupting normal cellular function. Preclinical studies of VVD-159642 give us confidence in its potential to inhibit tumor growth while avoiding the on-target toxicities that have limited prior attempts to drug this important target. In addition to providing a more tolerable alternative to current therapies, we believe that VVD-159642 has potential to treat a broad patient population, including in both RAS-mutant and HER2-overexpressed tumors, and may deliver increased efficacy in combination with other RAS/MAPK pathway inhibitors.” “We’re excited to bring our fourth innovative oncology asset into the clinic, which not only represents continued validation of Vividion’s covalent-first chemoproteomics platform but also provides a potential new treatment option for patients with RAS-driven cancers,” said Aleksandra Rizo M.D., Ph.D., Chief Executive Officer of Vividion. “The team at Vividion is rapidly advancing scientific innovations into clinical development that have the potential to address multiple devastating diseases not reachable by current therapies,” said Christian Rommel, Ph.D., Head of Research and Development at Bayer’s Pharmaceuticals Division. “The initiation of this clinical trial marks a significant step forward in leveraging Vividion’s innovative drug discovery approach to target a highly relevant signaling pathway and bring a potential new treatment option to people suffering from difficult-to-treat cancers.” Vividion also has ongoing Phase I trials evaluating an oral KEAP1 activator in solid tumors and oral STAT3 inhibitor in solid and hematologic malignancies. The company is advancing multiple innovative drug discovery programs toward the clinic and has a rich pipeline of opportunities emerging in early discovery in the fields of oncology and immunology. About Vividion Vividion Therapeutics, Inc., a wholly owned and independently operated subsidiary of Bayer AG, is a clinical stage biopharmaceutical company utilizing novel discovery technologies to unlock high value, traditionally undruggable targets with precision therapeutics for devastating cancers and immune disorders. The company’s platform has enabled it to identify hundreds of previously unknown functional pockets on well-validated protein targets implicated in a wide range of diseases, while simultaneously identifying compounds from its proprietary covalent chemistry library that interact in a highly selective manner with those pockets. The company is leveraging its proprietary chemoproteomic platform to advance a diversified pipeline of highly selective small molecule therapeutics targeting high value, traditionally undruggable targets in oncology and immunology. For more information, please visit www.vividion.com . About Bayer Bayer is a global enterprise with core competencies in the life science fields of health care and nutrition. In line with its mission, “Health for all, Hunger for none,” the company’s products and services are designed to help people and the planet thrive by supporting efforts to master the major challenges presented by a growing and aging global population. Bayer is committed to driving sustainable development and generating a positive impact with its businesses. At the same time, the Group aims to increase its earning power and create value through innovation and growth. The Bayer brand stands for trust, reliability and quality throughout the world. In fiscal 2024, the Group employed around 93,000 people and had sales of 46.6 billion euros. R&D expenses amounted to 6.2 billion euros. For more information, go to www.bayer.com . Find more information at https://pharma.bayer.com/ Follow us on Facebook: http://www.facebook.com/bayer SOURCE: Bayer

Phase 1

04 Apr 2025

·www.biospace.com

Amgen Wins Expansion for Uplizna as First Drug for IgG4-Related Disease

iStock, JHVEPhoto In the Phase III MITIGATE trial, Uplizna cut IgG4-related disease flares by 84% versus placebo. The FDA approved Amgen ’s anti-CD19 therapy Uplizna Thursday for use in patients with IgG4-related disease. Uplizna is the “first and only treatment” approved for this indication, according to the pharma’s statement. Uplizna’s label expansion is backed by data from the Phase III MITIGATE trial. Amgen first presented data from the study in November 2024, touting an 87% drop in the risk of disease-related flares versus placebo. Over 52 weeks of follow-up, seven of 68 Uplizna-treated patients experienced flares, as opposed to 40 of 67 placebo counterparts. Amgen called this effect highly statistically significant. In addition, 57.4% of patients in the Uplizna arm achieved complete remission at 52 weeks, versus 22.4% in the placebo group. Nearly 90% of Uplizna-treated participants no longer needed glucocorticoid treatment, versus 37.3% of placebo patients. After just 8 weeks of treatment, the Uplizna group saw a tenfold reduction in total glucocorticoid use as opposed to placebo. Designed to be delivered intravenously, Uplizna is a humanized monoclonal antibody that binds to the CD19 protein, typically found on the surface of certain immune cells, in turn depleting both immature and mature B cells. This mechanism allows Uplizna to target an underlying pathological pathway of IgG4-related disease, a condition characterized by organ damage due to massive infiltration of B cells into tissues. In Amgen’s news release, R&D Head Jay Bradner called Uplizna’s expansion into IgG4-related disease a “significant turning point” for patients and physicians, “who now have a proven treatment that targets a key driver of disease.” Uplizna is also approved for the treatment of neuromyelitis optica spectrum disorder and is being studied for generalized myasthenia gravis. Last month, Amgen posted 52-week Phase III findings, showing that Uplizna improved activities of daily living in a specific subset of patients, as well as easing disease activity versus placebo. Amgen is planning to Uplizna’s approval in this indication, with a submission planned for the first half of this year. Earlier this year, Amgen cleared another regulatory hurdle when its KRAS blocker Lumakras won the FDA’s blessing for use in colorectal cancer. The label expansion, which came in January, was a pleasant surprise to the pharma, especially since its Phase III CodeBreaK 300 trial failed to demonstrate a significant improvement in survival for Lumakras versus an investigator’s choice of treatment. The FDA’s approval of Lumakras in colorectal cancer was based on progression-free survival findings—the “major efficacy outcome” of CodeBreaK 300, as per the regulator—which improved significantly in patients who were given Lumakras plus Vectibix. Lumakras is also approved for non-small cell lung cancer, as per its label .

Phase 3Clinical ResultDrug Approval

01 Apr 2025

·ir.revmed.com

Revolution Medicines to Deliver Multiple Presentations at the 2025 American Association for Cancer Research (AACR) Annual Meeting

REDWOOD CITY, Calif., April 01, 2025 (GLOBE NEWSWIRE) -- Revolution Medicines, Inc. (Nasdaq: RVMD), a late-stage clinical oncology company developing targeted therapies for patients with RAS-addicted cancers, today announced 11 oral and poster presentations will be featured at the American Association for Cancer Research (AACR) Annual Meeting in Chicago, held from April 25 – 30, 2025. The first clinical data in non-small cell lung cancer from the Phase 1 study of zoldonrasib, a RAS(ON) G12D-selective inhibitor, will be featured in a late breaking oral presentation. Details of the abstracts are listed below: Revolution Medicines Oral Presentations: Title: Preliminary safety and antitumor activity of zoldonrasib (RMC-9805), an oral, RAS(ON) G12D-selective, tri-complex inhibitor in patients with KRAS G12D non-small cell lung cancer (NSCLC) from a Phase 1 study in advanced solid tumors Presenter: Kathryn Arbour, M.D., Memorial Sloan Kettering Cancer Center Abstract Number: CT019 Session: New Frontiers in Precision Oncology Date/Time: April 27; 5:00 p.m. – 5:15 p.m. CST Title: Discovery of RMC-5127, an oral, RAS(ON) G12V-selective, noncovalent, tri-complex inhibitor Presenter: Anne Edwards, Ph.D. Abstract Number: ND06 Session: New Drugs on the Horizon: Part 2 Date/Time: April 27; 3:25 p.m. – 3:40 p.m. CST Revolution Medicines Poster Presentations: Title: Early reduction in circulating tumor DNA (ctDNA) is associated with clinical activity of daraxonrasib (RMC-6236) in RAS mutant non-small cell lung cancer (NSCLC) Presenter: Jia Luo, M.D., Dana-Farber Cancer Institute Abstract Number: LB218 Session: Late-Breaking Research: Clinical Research 1 Date/Time: April 28; 2:00 p.m. – 5:00 p.m. CST Title: Mechanisms of resistance to the RAS(ON) multi-selective inhibitor daraxonrasib (RMC-6236) in RAS mutant PDAC and potential resolution with RAS(ON) combination therapies Presenter: Mallika Singh, Ph.D. Abstract Number: LB281 Session: Late-Breaking Research: Experimental and Molecular Therapeutics 3 Date/Time: April 29; 9:00 a.m. – 12:00 p.m. CST Title: Combination of RAS(ON) mutant-selective and multi-selective inhibitors sensitizes immune-refractory, RAS-driven preclinical models to immunotherapy Presenter: Mariela Moreno Ayala, Ph.D. Abstract Number: 6046 Session: Adaptive Immunity in Tumors / Oncogenic Pathway-Mediated Regulation of Inflammation and Tumor Immunity Date/Time: April 29; 2:00 p.m. – 5:00 p.m. CST Collaborator Presentations Title: Distinct regulation of Cyclin D mediates heterogenous response to RAS inhibition in colorectal cancer models Presenter: Philip Choi, M.D., Ph.D., Memorial Sloan Kettering Cancer Center Abstract Number: LB293 Session: Late-Breaking Research: Experimental and Molecular Therapeutics 3 Date/Time: April 29; 9:00 a.m. – 12:00 p.m. CST Title: Combining RAS(ON) G12C-selective and RAS(ON) multi-selective inhibitors overcomes sotorasib resistance driven by KRAS G12C amplification or NRAS G13R mutation Presenter: Hitendra Singh Solanki, Ph.D., Moffitt Cancer Center Abstract Number: 5512 Session: Drug Resistance in Molecular Targeted Therapies 3 Date/Time: April 29; 2:00 p.m. – 5:00 p.m. CST Title: A RAS(ON) multi-selective inhibitor combination therapy triggers long-term tumor control through senescence-associated tumor-immune equilibrium in preclinical models of PDAC Presenter: Caroline Broderick, Ph.D., Memorial Sloan Kettering Cancer Center Abstract Number: 5336 Session: CDK Inhibitors Date/Time: April 29; 2:00 p.m. – 5:00 p.m. CST Title: Preclinical evaluation of RMC-7977, a multi-selective RAS(ON) inhibitor, as a therapeutic strategy for KRAS-mutant cholangiocarcinoma Presenter: Jingjing Jiang, Ph.D. Abstract Number: 5691 Session: Oncogenes, Tumor Suppressor Genes, and Gene Products as Targets for Therapy 2 Date/Time: April 29; 2:00 p.m. – 5:00 p.m. CST Title: Mechanisms of resistance to RAS-GTP inhibition in pancreatic cancer Presenter: Joshua H. Choe, Dana-Farber Cancer Institute Abstract Number: 5507 Session: Drug Resistance in Molecular Targeted Therapies 3 Date/Time: April 29; 2:00 p.m. – 5:00 p.m. CST Title: T-cell dependency of tumor regressions and complete responses with RAS(ON) multi-selective inhibition in preclinical models of PDAC Presenter: Margo I. Orlen, Penn Medicine Abstract Number: 6405 Session: Checkpoints and Modulators of Tumor Microenvironment Date/Time: April 29; 3:25 p.m. – 3:40 p.m. CST About Revolution Medicines, Inc.Revolution Medicines is a late-stage clinical oncology company developing novel targeted therapies for patients with RAS-addicted cancers. The company’s R&D pipeline comprises RAS(ON) inhibitors designed to suppress diverse oncogenic variants of RAS proteins. The company’s RAS(ON) inhibitors daraxonrasib (RMC-6236), a RAS(ON) multi-selective inhibitor; elironrasib (RMC-6291), a RAS(ON) G12C-selective inhibitor; and zoldonrasib (RMC-9805), a RAS(ON) G12D-selective inhibitor, are currently in clinical development. The company anticipates that RMC-5127, a RAS(ON) G12V-selective inhibitor, will be its next RAS(ON) inhibitor to enter clinical development. Additional development opportunities in the company’s pipeline focus on RAS(ON) mutant-selective inhibitors, including RMC-0708 (Q61H) and RMC-8839 (G13C). For more information, please visit www.revmed.com and follow us on LinkedIn. Revolution Medicines Media & Investor Contact:media@revmed.cominvestors@revmed.com

Phase 1AACRImmunotherapy

100 Deals associated with Sotorasib

External Link

KEGG	Wiki	ATC	Drug Bank
-	Sotorasib	L01XE	DB15569

R&D Status

Approved

10 top approved records.

to view more data

Indication	Country/Location	Organization	Date
KRAS G12C mutant Colorectal Cancer	United States	Amgen, Inc.	16 Jan 2025
KRAS G12C mutant Non-small Cell Lung Cancer	United States	Amgen, Inc.	28 May 2021

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Non-Small Cell Lung Cancer	Phase 3	United States	Amgen, Inc.	16 Nov 2023
Non-Small Cell Lung Cancer	Phase 3	China	Amgen, Inc.	16 Nov 2023
Non-Small Cell Lung Cancer	Phase 3	Japan	Amgen, Inc.	16 Nov 2023
Non-Small Cell Lung Cancer	Phase 3	Argentina	Amgen, Inc.	16 Nov 2023
Non-Small Cell Lung Cancer	Phase 3	Australia	Amgen, Inc.	16 Nov 2023
Non-Small Cell Lung Cancer	Phase 3	Austria	Amgen, Inc.	16 Nov 2023
Non-Small Cell Lung Cancer	Phase 3	Belgium	Amgen, Inc.	16 Nov 2023
Non-Small Cell Lung Cancer	Phase 3	Brazil	Amgen, Inc.	16 Nov 2023
Non-Small Cell Lung Cancer	Phase 3	Bulgaria	Amgen, Inc.	16 Nov 2023
Non-Small Cell Lung Cancer	Phase 3	Canada	Amgen, Inc.	16 Nov 2023

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


AACR2025	Not Applicable	KRAS G12C	-	Nanosuspension with sotorasib	wtlerltlao(ztvogllldo) = ktrzokofwz hhaumxgizc (hismxfrfty, 1346.66) View more	-	28 Apr 2025
NCT05198934 (CodeBreaK 300, FDA_CDER) Manual	Phase 3	KRAS G12C mutant Colorectal Cancer KRAS G12C	107	LUMAKRAS 960 mg + Panitumumab	tpfbbhmvdz(ssqrfurrnz) = htiedkvyfd hlkwzgbdbc (zzryjtcuaw, 4.2 - 6.3) View more	Positive	16 Jan 2025
				SOC (trifluridine/tipiracil or regorafenib)regorafenib)	tpfbbhmvdz(ssqrfurrnz) = xwiixgxyfl hlkwzgbdbc (zzryjtcuaw, 1.9 - 3.9) View more
NCT05074810 (RAMP 203, BusinessWire) Manual	Phase 1/2	KRAS G12C mutant Non-small Cell Lung Cancer KRAS G12C	3	Defactinib，Avutometinib, sotorasib	dwebfryorx(dpehgsfkrg) = None nhdfhsbtjw (umxpllcpsj ) View more	Positive	18 Dec 2024
NCT04185883 (CodeBreaK 101, ESMO2024) Manual	Phase 1	KRAS G12C mutant Colorectal Cancer First line KRAS G12C–mutated	40	Sotorasib (soto) + Panitumumab (pani) + FOLFIRI	rbgynbggng(eblpblnzkr) = fztaokguyd ryhffaypzj (nmcazrlpmb ) View more	Positive	15 Sep 2024
ESMO2024 Manual	Not Applicable	Non-Small Cell Lung Cancer	125	Sotorasib	xbrtsgsvnx(pluobowsit) = vxcgzzypvr mtqsrijcdn (ldcgvpozqc ) View more	Positive	14 Sep 2024
				Sotorasib (CodeBreak 100)	xbrtsgsvnx(pluobowsit) = jorwuhavho mtqsrijcdn (ldcgvpozqc ) View more
NCT04303780 \| NCT04380753 \| NCT04185883 \| NCT03600883 (CodeBreaK 100, ESMO2024) Manual	Not Applicable	KRAS G12C mutant Non-small Cell Lung Cancer KRAS G12C	549	Sotorasib 960 mg once daily	iexgdgikun(cwctftpwmk) = asyfslvtpw kehbegfpjo (klaogctwfb ) View more	Positive	14 Sep 2024
WCLC2024 \| Pubmed Manual	Not Applicable	KRAS G12C mutant Non-small Cell Lung Cancer Second line KRAS G12c-Mutated	383	Sotorasib	jchayiwgah(ihkhlstldh) = ekaslnxsof totxtolqts (zsogbyrnki, 7.6 - 16.3) View more	Positive	09 Sep 2024
				Docetaxel	jchayiwgah(ihkhlstldh) = bzhcunakib totxtolqts (zsogbyrnki, 4.2 - 11.0) View more
WCLC2024 Manual	Not Applicable	KRAS G12C mutant Non-small Cell Lung Cancer KRAS G12C	150	Sotorasib 960 mg once daily	ucaeejfjjt(dwzamlgngm) = pfwtewxeim coouxgdthd (isxdpfpcxu, 5.0 - 7.3) View more	Positive	09 Sep 2024
				Sotorasib 960 mg once daily (with CNS metastases)	doihqcqrvc(turvbugare) = kfwqoxnvms zcbyncsvrz (liabujoigp, 7.2 - 12.7) View more
WCLC2024	Phase 3	metastatic non-small cell lung cancer KRAS G12C+	-	Divarasib	kunuhcqkgu(jjwkeeswpj) = xtwczpypzm ekhiidqckp (rutmoyhjkj, 39.6 - 72.2) View more	-	09 Sep 2024
WCLC2024 Manual	Not Applicable	KRAS G12C mutant Non-small Cell Lung Cancer	8	KRAS G12Ci (G12Ci as first-line therapy)	yrocdedcvm(alvmjkyrqb) = qwxvexqnsr bgvsdcansd (lxzmbenwsc ) View more	-	07 Sep 2024
				KRASG12Ci	yrocdedcvm(alvmjkyrqb) = phxwgyzeui bgvsdcansd (lxzmbenwsc, 2.77 - 35.23) View more

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