RegulationBreakthrough Therapy (US), Fast Track (US), Accelerated Approval (US), Orphan Drug (US), Breakthrough Therapy (CN), Orphan Drug (AU), Conditional marketing approval (US)

Structure

Molecular FormulaC30H30F2N6O3

InChIKeyNXQKSXLFSAEQCZ-SFHVURJKSA-N

CAS Registry2252403-56-6

Clinical Trials associated with Sotorasib

NCT05638295 / RecruitingPhase 2IIT

A Randomized Phase II Study of AMG 510 (Sotorasib) With or Without Panitumumab in Advanced Solid Tumors: A ComboMATCH Treatment Trial

This phase II ComboMATCH treatment trial tests how well AMG 510 (sotorasib) with or without panitumumab works in treating patients with KRAS G12C mutant solid tumors that may have spread from where it first started to nearby tissue, lymph nodes, or distant parts of the body (advanced). Sotorasib is in a class of medications called KRAS inhibitors. It works by blocking the action of the abnormal protein that signals cancer cells to multiply. This helps stop or slow the spread of cancer cells. Panitumumab is in a class of medications called monoclonal antibodies. It works by slowing or stopping the growth of cancer cells. Giving combination panitumumab and sotorasib may kill more tumor cells in patients with advanced solid tumors with KRAS G12C mutation.

Start Date14 Oct 2024

Sponsor / Collaborator

National Cancer Institute

NCT06061523 / WithdrawnPhase 1

A Phase I, Open-label, Randomized Crossover Study to Evaluate the Relative Bioavailability and the Effect of Food for Sotorasib Tablets in Healthy Participants

The primary objectives of the study are to compare the pharmacokinetics (PK) and demonstrate relative bioavailability of sotorasib administered as 4 oral tablets (test) to sotorasib administered as 8 oral tablets (reference) and to assess the effect of food on the PK of sotorasib administered as 4 oral tablets.

Start Date15 Jul 2024

Sponsor / Collaborator

Amgen, Inc.

NCT06252649 / Not yet recruitingPhase 3

Phase 3 Multicenter, Randomized, Open-label, Active-controlled Study of Sotorasib, Panitumumab and FOLFIRI Versus FOLFIRI With or Without Bevacizumab-awwb for Treatment-naïve Subjects With Metastatic Colorectal Cancer With KRAS p.G12C Mutation (CodeBreaK 301)

The aim of this study is to compare progression free survival (PFS) in treatment-naïve Participants with KRAS p.G12C mutated metastatic colorectal cancer (mCRC) receiving sotorasib, panitumumab and FOLFIRI vs FOLFIRI with or without bevacizumab-awwb.

Start Date01 Jul 2024

Sponsor / Collaborator

Amgen, Inc.

100 Clinical Results associated with Sotorasib

100 Translational Medicine associated with Sotorasib

100 Patents (Medical) associated with Sotorasib

267

Literatures (Medical) associated with Sotorasib

01 Mar 2024·Bioorganic chemistry

Multiple medicinal chemistry strategies of targeting KRAS: State-of-the art and future directions

Review

Author: Shang, Yanguo ; Wang, Jinxin ; Hao, Qingjing ; Shen, Tao ; Fu, Shengnan ; Ying, Hanjie

KRAS is the most frequently mutated oncogene and drives the development and progression of malignancies, most notably non-small cell lung cancer (NSCLS), pancreatic ductal adenocarcinoma (PDAC) and colorectal cancer (CRC). However, KRAS proteins have maintained the reputation of being "undruggable" due to the lack of suitable deep pockets on its surface. One major milestone for KRAS inhibition was the discovery of the covalent inhibitors bond to the allosteric switch-II pocket of the KRAS^G12C protein. To date, the FDA has approved two KRAS^G12C inhibitors, sotorasib and adagrasib, for the treatment of patients with KRAS^G12C-driven cancers. Researchers have paid close attention to the development of inhibitors for other KRAS mutations and upstream regulatory factors. The KRAS targeted drug discovery has entered a state of rapid development. This article has aimed to present the current state of the art of drug development in the KRAS field. We systematically summarize recent advances in the discovery and optimization processes of direct KRAS inhibitors (including KRAS^G12C, KRAS^G12D, KRAS^G12A and KRAS^G12R inhibitors), indirect KRAS inhibitors (SOS1 and SHP2 inhibitors), pan-KRAS inhibitors, as well as proteolysis-targetingchimeras degrades and molecular chaperone modulators from the perspective of medicinal chemistry. We also discuss the current challenges and opportunities of KRAS inhibition and hope to shed light on future KRAS drug discovery.

02 Feb 2024·The oncologist

Increased KRAS G12C Prevalence, High Tumor Mutational Burden, and Specific Mutational Signatures Are Associated With MUTYH Mutations: A Pan-Cancer Analysis

Article

Author: Disel, Umut ; Pham, Tim ; Kurzrock, Razelle ; Fleischmann, Zoe ; Sokol, Ethan S ; Anu, R I ; Sivakumar, Smruthy

Abstract:

The aim of this study was to determine the pan-cancer landscape of MUTYH alterations and the relationship between MUTYH mutations and potentially actionable biomarkers such as specific genomic alterations, tumor mutational burden, and mutational signatures. We used a large pan-cancer comprehensive genomic dataset from patients profiled (tissue next generation sequencing) during routine clinical care. Overall, 2.8% of 229 120 solid tumors had MUTYH alterations, of which 55% were predicted germline. Thirty tumor types had a 2% or greater MUTYH mutation rate. MUTYH-altered versus -WT cancers had significantly higher tumor mutational burden and more frequent alterations in KRAS G12C, but not in KRAS in general; these observations were statistically significant, especially in colorectal cancers. Across cancers, PD-L1 expression levels (immunohistochemistry) were not associated with MUTYH alteration status. In silico computation demonstrated that MUTYH mutational signatures are associated with higher levels of hydrophobicity (which may reflect higher immunogenicity of neoantigens) relative to several other signature types such as microsatellite instability. Survival of patients with MUTYH-altered versus -WT tumors was similar. In conclusion, comprehensive genomic profiling suggests that several features of MUTYH-altered cancers may be pharmacologically targetable. Drugs such as sotorasib (targeting KRAS G12C) and immune checkpoint inhibitors, targeting the increased mutational load and higher neo-antigen hydrophobicity/immunogenicity merit investigation in MUTYH-mutated malignancies.

01 Feb 2024·Pharmacological research

Outcomes following KRASG12C inhibitor treatment in patients with KRASG12C-mutated solid tumors: A systematic review and meta-analysis

Review

Author: Gao, Yi-Bo ; He, Jie ; Chen, Qi-An ; Zhou, Xiao-Xiang ; Lin, Wei-Hao ; Cao, Zheng ; Feng, Xiao-Li

OBJECTIVE:

To assess the efficacy and safety of FDA-approved KRAS^G12C inhibitors in patients with KRAS^G12C-mutated solid tumors.

METHODS:

We searched PubMed, EMBASE, Cochrane Library, and major international conferences for clinical trials published in English up to March 6, 2023. Clinical trials investigating sotorasib or adagrasib and reporting the clinical outcomes of the objective response rate (ORR), disease control rate (DCR), or incidence rate of grade ≥ 3 adverse events (AEs) were eligible. The primary endpoint was the ORR. Secondary endpoints included the DCR, incidence rate of grade ≥ 3 AEs, and odds ratio (OR) of the ORR between patients with or without co-mutation. The Random-effects model was applied for the outcomes of interest.

RESULTS:

18 studies with 1224 patients were included in this meta-analysis. The pooled ORR, DCR, and incidence rate of grade ≥ 3 AEs were 31 % (95 % CI, 25-37 %), 86 % (95 % CI, 82-89 %), and 29 % (95 % CI, 23-36 %), respectively. KRAS^G12C-mutated NSCLC patients with a co-mutation of KEAP1 exhibited a worse ORR than those with wild-type KEAP1 (OR: 0.35, 95 % CI: 0.16-0.77).

CONCLUSIONS:

This study provided a comprehensive understanding of the efficacy and safety of KRAS^G12C inhibitors in treating solid tumors and identified KEAP1 mutation as a potential predictive biomarker of inferior response in patients treated with KRAS^G12C inhibitors. These findings may assist in the design of future clinical trials for identifying populations that may benefit from KRAS^G12C inhibitor treatment.

298

News (Medical) associated with Sotorasib

01 Jul 2024

·www.biospace.com

Verastem Oncology Announces Addition to Russell 3000® and Russell Microcap® Indexes

BOSTON--(BUSINESS WIRE)-- Verastem Oncology (Nasdaq: VSTM), a biopharmaceutical company committed to advancing new medicines for patients with cancer, today announced that in connection with the 2024 Russell U.S. Indexes annual reconstitution, the company will be added to the Russell 3000® and Russell Microcap® Indexes, effective at the open of U.S. equity markets today, Monday, July 1, 2024. “The recognition and increased exposure of being added to the Russell Indexes underscore the recent progress we’ve made across our pipeline, which includes bringing avutometinib in combination with defactinib one step closer to being a potential new treatment option for patients with recurrent low-grade serous ovarian cancer in the U.S.,” said Dan Paterson, president and chief executive officer of Verastem Oncology. “We remain on track to announce mature data from RAMP 201 and complete our rolling NDA submission in the second half of 2024 while advancing our other clinical programs in metastatic pancreatic cancer and non-small cell lung cancer. Now that GenFleet has initiated the Phase 1/2 clinical trial in China for GFH375/VS-7375, a potent and selective oral KRAS G12D (ON/OFF) inhibitor, we look forward to leveraging this data to accelerate a path forward in the U.S. and rest of world.” The annual Russell indexes reconstitution captures the 4,000 largest U.S. stocks as of Thursday, April 30, 2024, ranking them by total market capitalization. Russell indexes are widely used by investment managers and institutional investors for index funds and as benchmarks for active investment strategies. According to the data as of the end of December 2023, about $10.5 trillion assets are benchmarked against the Russell U.S. indexes, which belong to FTSE Russell, a prominent global index provider. For more information on the Russell 3000® Index and the Russell indexes reconstitution, go to the “Russell Reconstitution” section of the FTSE Russell website. About Verastem Oncology Verastem Oncology (Nasdaq: VSTM) is a late-stage development biopharmaceutical company committed to the development and commercialization of new medicines to improve the lives of patients diagnosed with cancer. Our pipeline is focused on RAS/MAPK-driven cancers, specifically novel small molecule drugs that inhibit critical signaling pathways in cancer that promote cancer cell survival and tumor growth, including RAF/MEK inhibition and FAK inhibition. For more information, please visit and follow us on LinkedIn. About FTSE Russell FTSE Russell is a leading global provider of benchmarking, analytics, and data solutions for investors, giving them a precise view of the market relevant to their investment process. A comprehensive range of reliable and accurate indexes provides investors worldwide with the tools they require to measure and benchmark markets across asset classes, styles, or strategies. FTSE Russell index expertise and products are used extensively by institutional and retail investors globally. For over 30 years, leading asset owners, asset managers, ETF providers and investment banks have chosen FTSE Russell indexes to benchmark their investment performance and create ETFs, structured products, and index-based derivatives. FTSE Russell is focused on applying the highest industry standards in index design and governance, employing transparent rules-based methodology informed by independent committees of leading market participants. FTSE Russell fully embraces the IOSCO Principles, and its Statement of Compliance has received independent assurance. Index innovation is driven by client needs and customer partnerships, allowing FTSE Russell to continually enhance the breadth, depth and reach of its offering. FTSE Russell is wholly owned by London Stock Exchange Group. For more information, visit . Forward Looking Statements This press release includes forward-looking statements about, among other things, Verastem Oncology’s programs and product candidates, strategy, future plans and prospects, including statements related to the impact of the company’s addition to the Russell 3000® and Russell Microcap® Indexes, the expected outcome and benefits of collaborations, including with GenFleet Therapeutics (Shanghai), Inc. (“GenFleet”), the timing of commencing and completing trials, including topline data reports, interactions with regulators, the potential for the commercialization of product candidates and potential for additional development programs involving Verastem Oncology’s lead compound. The words "anticipate," "believe," "estimate," "expect," "intend," "may," "plan," "predict," "project," "target," "potential," "will," "would," "could," "should," "continue," "can, " "promising" and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. Forward-looking statements are not guarantees of future performance and are subject to risks and uncertainties that could cause actual results to differ materially from those expressed or implied in such statement. Applicable risks and uncertainties include the risks and uncertainties, among other things, regarding: the success in the development and potential commercialization of our product candidates, including avutometinib in combination with other compounds, including defactinib, LUMAKRAS and others; the uncertainties inherent in research and development, such as negative or unexpected results of clinical trials, the occurrence or timing of applications for our product candidates that may be filed with regulatory authorities in any jurisdictions; whether and when regulatory authorities in any jurisdictions may approve any such applications that may be filed for our product candidates, and, if approved, whether our product candidates will be commercially successful in such jurisdictions; our ability to obtain, maintain and enforce patent and other intellectual property protection for our product candidates; the scope, timing, and outcome of any legal proceedings; decisions by regulatory authorities regarding trial design, labeling and other matters that could affect the timing, availability or commercial potential of our product candidates; whether preclinical testing of our product candidates and preliminary or interim data from clinical trials will be predictive of the results or success of ongoing or later clinical trials; that the timing, scope and rate of reimbursement for our product candidates is uncertain; the market opportunities of our drug candidates are based on internal and third-party estimates which may prove to be incorrect; that third-party payors (including government agencies) may not reimburse; that there may be competitive developments affecting our product candidates; that data may not be available when expected; that enrollment of clinical trials may take longer than expected, which may delay our development programs, including delays in submission or review by the FDA of our NDA submission in recurrent KRAS mutant LGSOC if enrollment in our confirmatory trial is not well underway at the time of submission; that our product candidates will cause adverse safety events and/or unexpected concerns may arise from additional data or analysis, or result in unmanageable safety profiles as compared to their levels of efficacy; that we maybe unable to successfully validate, develop and obtain regulatory approval for companion diagnostic tests for our product candidates that require or would commercially benefit from such tests, or experience significant delays in doing so; that the mature RAMP 201 data and associated discussions with the FDA may not support the scope of our rolling NDA submission for the avutometinib and defactinib combination in LGSOC, including with respect to KRAS wild type LGSOC; that our product candidates may experience manufacturing or supply interruptions or failures; that any of our third-party contract research organizations, contract manufacturing organizations, clinical sites, or contractors, among others, who we rely on fail to fully perform; that we face substantial competition, which may result in others developing or commercializing products before or more successfully than we do which could result in reduced market share or market potential for our product candidates; that we will be unable to successfully initiate or complete the clinical development and eventual commercialization of our product candidates; that the development and commercialization of our product candidates will take longer or cost more than planned, including as a result of conducting additional studies or our decisions regarding execution of such commercialization; that we may not have sufficient cash to fund our contemplated operations , including certain of our product development programs; that we may not attract and retain high quality personnel; that we or Chugai Pharmaceutical Co., Ltd. will fail to fully perform under the avutometinib license agreement; that our total addressable and target markets for our product candidates might be smaller than we are presently estimating; that Secura Bio, Inc. will fail to fully perform under the asset purchase agreement with Secura Bio, Inc., including in relation to milestone payments; that we will not see a return on investment on the payments we have and may continue to make pursuant to the collaboration and option agreement with GenFleet or that GenFleet will fail to fully perform under the agreement; that we may not be able to establish new or expand on existing collaborations or partnerships, including with respect to in-licensing of our product candidates, on favorable terms, or at all; that we may be unable to obtain adequate financing in the future through product licensing, co-promotional arrangements, public or private equity, debt financing or otherwise; that we will not pursue or submit regulatory filings for our product candidates; and that our product candidates will not receive regulatory approval, become commercially successful products, or result in new treatment options being offered to patients. As a result of these and other factors, we may not achieve the plans, intentions or expectations disclosed in our forward-looking statements, and you should not place undue reliance on our forward-looking statements. Other risks and uncertainties include those identified under the heading “Risk Factors” in the Company’s Annual Report on Form 10-K for the year ended December 31, 2023, as filed with the Securities and Exchange Commission (SEC) on March 14, 2024, and in any subsequent filings with the SEC, which are available at and .

24 Jun 2024

·www.fiercepharma.com

BMS, Mirati's Krazati cements lead over Amgen's Lumakras with FDA approval in colorectal cancer

Aside from moving into a second indication to Lumakras’ one, Krazati further cemented its lead in the KRAS race this past March when BMS unveiled positive confirmatory results from the late-stage KRYSTAL-12 study in lung cancer. Despite coming to market second, Bristol Myers Squibb’s Mirati Therapeutics-inherited cancer med Krazati has gained the lead on its Amgen rival Lumakras in a heated KRAS race. Late Friday, the U.S. FDA granted an accelerated approval for BMS’ KRAS inhibitor Krazati plus Eli Lilly’s Erbitux (cetuximab) to treat certain chemotherapy-experienced adults with KRAS-mutated locally advanced or metastatic colorectal cancer (CRC). Given that the approval is accelerated, BMS may have to further prove Krazati’s merit in CRC in a confirmatory trial to keep hold of the green light. The new nod comes after Krazati’s initial approval in previously treated KRAS G12C-mutated non-small cell lung cancer (NSCLC) in Dec. 2022. Krazati, also known as adagrasib, was the second KRAS-targeting drug to hit the U.S. market behind Lumakras, which snagged its initial approval in NSCLC in May 2021. BMS got its hands on Krazati when it agreed to buy out Mirati for around $4.8 billion last fall. Bristol closed the transaction in late January. CRC with a KRAS G12C mutation occurs in approximately 3% to 4% of colorectal cancer patients and has historically proven difficult to treat, according to Rona Yaeger, M.D., gastrointestinal oncologist and early drug development specialist at Memorial Sloan Kettering Cancer Center. The FDA based its approval on early results from Krazati’s 94-patient, phase 1/2 KRYSTAL-1 open-label study, in which the drug was administered in 600mg tablets twice a day along with Erbitux either weekly or biweekly, the FDA explained in a separate release. In the trial, the Krazati combo reached a confirmed objective response rate (ORR) of 34%--meeting its primary endpoint—and charted a median duration of response (DOR) of 5.8 months. Thirty-one percent of patients who responded to Krazati had a DOR of at least half-a-year, the FDA noted. Current late-line standard-of-care medicines in CRC yield limited objective response rates of around 1% to 6% after progression on chemotherapy, BMS pointed out. Aside from moving into a second indication to Lumakras’ one, Krazati further cemented its lead in the KRAS race this past March when BMS unveiled confirmatory results from the late-stage KRYSTAL-12 study that found the med significantly reduced the risk of tumor progression or death versus chemotherapy in certain NSCLC patients. Krazati’s confirmatory win marked another blow to Lumakras after Amgen recently applied for a full approval of its rival KRAS inhibitor leveraging progression-free survival data from the phase 3 CodeBreaK 200 trial. Problem was, the FDA figured the study’s results couldn’t be reliably interpreted, and a group of external advisers agreed. Despite this, the FDA has let Lumakras stay on the market while Amgen runs another confirmatory study. The California-based company expects that to be done no later than Feb. 2028. Meanwhile, Amgen is also gunning for a Lumakras approval in CRC. The company in October reported results from its phase 3 CodeBreaK 300 trial showing that 960mg Lumakras plus Vectibix extended patients' median progression-free survival to 5.6 months versus 2.2 months for standard treatments in chemo-refractory KRAS G12C colorectal cancer. Krazati, during its first earnings quarter under BMS’ wing, snared $21 million over the first three months of 2024.

Clinical ResultDrug ApprovalPhase 3Acquisition

06 Jun 2024

·www.biospace.com

BridgeBio Oncology Therapeutics announces first patient dosed with BBO-8520 in the Ph. 1 ONKORAS-101 trial for KRASG12C NSCLC

- The first patient has been dosed in the ONKORAS-101 trial for the study of BBO-8520 in adult subjects with KRASG12C non-small cell lung cancer - BBO-8520 is a first-in-class orally bioavailable and highly potent small molecule direct inhibitor of KRASG12C that binds to the Switch II pocket in both the GTP-bound (ON) and GDP-bound (OFF) state conformations of KRASG12C - BBO-8520 is expected to meaningfully improve outcomes for patients with KRASG12C driven malignancies by providing optimal target coverage and addressing mechanisms of adaptive resistance to first generation KRASG12C (OFF) state inhibitors SOUTH SAN FRANCISCO, Calif.--(BUSINESS WIRE)-- TheRas, Inc. d/b/a BridgeBio Oncology Therapeutics (“BBOT” or the “Company”), a clinical-stage biopharmaceutical company focused on RAS-pathway malignancies, has announced that the first patient has been dosed in the ONKORAS-101 trial for its lead program, BBO-8520. BBO-8520 is a first-in-class orally bioavailable and highly potent small molecule direct inhibitor of KRASG12C (ON) state. BBO-8520 binds covalently to the Switch II pocket in both the GTP-bound (ON) and GDP-bound (OFF) state conformations of KRASG12C, leading to rapid and sustained inhibition of KRASG12C activity. On dosing the first patient, Professor Benjamin Solomon, head of lung medical oncology at the Peter MacCallum Cancer Center, said, “We are excited to partner with BridgeBio Oncology Therapeutics to bring a transformative new therapy to patients. Non-small cell lung cancer is among the most prevalent malignancies globally and there is a significant need for new precision oncology medicines to improve outcomes for patients in the metastatic setting. BBO-8520 promises to have a substantial impact in improving outcomes and prognosis for this group of patients.” BBO-8520 was designed to inhibit the (ON) state to provide optimal target coverage and to address KRASG12C amplification and receptor tyrosine kinase activation - the two key mechanisms of adaptive resistance to current (OFF) state inhibitors. BBO-8520 drives substantial tumor growth inhibition in multiple preclinical models, even after emergence of resistance to sotorasib, an FDA approved (OFF) state inhibitor of KRASG12C. BBO-8520’s discovery was the result of a collaboration between the National Cancer Institute RAS Initiative at Frederick National Laboratory for Cancer Research, Lawrence Livermore National Laboratory, and BridgeBio Oncology Therapeutics. The ONKORAS-101 study will enroll patients pre-treated with first generation KRASG12C (OFF) inhibitors as well as patients with no prior KRASG12C targeted therapy experience. The trial will enroll across the US, Australia, Canada, and the EU. BridgeBio Oncology Therapeutics’ CEO, Eli Wallace, PhD, added, "The initiation of the Phase 1 clinical trial of BBO-8520 represents an important advancement for BBOT, as we are now a clinical-stage organization. We are grateful for the opportunity to offer patients with KRASG12C-driven lung cancer a targeted therapy that is expected to provide a significant improvement over current standards of care." About TheRas, Inc. d/b/a BridgeBio Oncology Therapeutics BridgeBio Oncology Therapeutics is a clinical-stage biopharmaceutical company advancing a next generation pipeline of novel small molecule therapeutics targeting RAS and PI3K malignancies. Initially formed as a subsidiary of BridgeBio, BridgeBio Oncology Therapeutics completed a $200M private financing with external investors in 2024 with the goal of improving outcomes for patients with cancers driven by the two most prevalent oncogenes in human tumors. For more information visit bridgebiooncology.com.

Phase 1

100 Deals associated with Sotorasib

External Link

KEGG	Wiki	ATC	Drug Bank
-	-	L01XE	DB15569

R&D Status

Approved

10 top approved records.

to view more data

Indication	Country/Location	Organization	Date
Advanced Lung Non-Small Cell Carcinoma	GB	Amgen, Inc.	03 Sep 2021
KRAS G12C mutant Non-small Cell Lung Cancer	US	Amgen, Inc.	28 May 2021

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Metastatic Colorectal Carcinoma	Phase 3	-	Amgen, Inc.	01 Jul 2024
Colorectal Cancer	Phase 3	US	-	25 Jan 2024
Non-Small Cell Lung Cancer	Phase 3	US	Amgen, Inc.	16 Nov 2023
Non-Small Cell Lung Cancer	Phase 3	CN	Amgen, Inc.	16 Nov 2023
Non-Small Cell Lung Cancer	Phase 3	JP	Amgen, Inc.	16 Nov 2023
Non-Small Cell Lung Cancer	Phase 3	AR	Amgen, Inc.	16 Nov 2023
Non-Small Cell Lung Cancer	Phase 3	AU	Amgen, Inc.	16 Nov 2023
Non-Small Cell Lung Cancer	Phase 3	AT	Amgen, Inc.	16 Nov 2023
Non-Small Cell Lung Cancer	Phase 3	BE	Amgen, Inc.	16 Nov 2023
Non-Small Cell Lung Cancer	Phase 3	BR	Amgen, Inc.	16 Nov 2023

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04185883 (CodeBreaK 101, ASCO2024)	Phase 1	Advanced Malignant Solid Neoplasm KRASG12C	40	Sotorasib 960 mg	rjkufhozuz(fjwxyixjco) = himqqqgxyg bsiipyrbtz (rxrkmucdgh ) View more	Positive	24 May 2024
NCT04185883 (CodeBreaK 101, ASCO2024)	Phase 1	KRASG12C	58	Sotorasib 960 mg QD plus carboplatin AUC 5 IV Q3W and pemetrexed 500 mg/m2IV Q3W	vlitrtydfr(lzcvkrxtld) = bcfxpirbfi yaxywshopk (vepigwyecc ) View more	Positive	24 May 2024
ASCO2024	Not Applicable	Second line KRASG12Cmutation	345	Sotorasib	rbwdkkupeb(sninbtdlss) = xkwtmpatqy pxwezmsqrm (qxwlevpjfb )	Positive	24 May 2024
NCT04887064 (CTgov)	Phase 1	Liver Diseases	20	sotorasib (Normal Hepatic Function)	hhwmyoqksb(mbcayegitd) = knmcbzkfht tbwsurbosh (gcqrvruvbq, twqgoymfvh - atgdwfkcmo) View more	-	19 Apr 2024
NCT04887064 (CTgov)	Phase 1	Liver Diseases	20	sotorasib (Moderate Hepatic Impairment)	hhwmyoqksb(mbcayegitd) = ccmeafjzla tbwsurbosh (gcqrvruvbq, toamimzmqv - jjalvxkywl) View more	-	19 Apr 2024
NCT04380753 (CTgov)	Phase 1	Solid tumor \| KRAS G12C mutation Solid Tumors	12	Sotorasib	qgdqxtflok(srmiyauuvr) = tuszjejtur ivrvjkpjyd (glyxkzkqvp, yeaggikkle - brirkennpp) View more	-	22 Mar 2024
NCT05497557 (CTgov)	Phase 1	-	16	Sotorasib (Sotorasib Alone)	acfwqnbukq(kjywbqdxkd) = krdwsmveyv rgkznoajoh (dgdoqmreal, hrazksygck - ezslfdkphx) View more	-	19 Jan 2024
NCT05497557 (CTgov)	Phase 1	-	16	Omeprazole+Sotorasib (Omeprazole Co-administered With Sotorasib)	acfwqnbukq(kjywbqdxkd) = webhbveban rgkznoajoh (dgdoqmreal, uxhjqjnovt - imajroaepu) View more	-	19 Jan 2024
NCT04185883 (CodeBreaK 101, ASCO_GI2024) Manual	Phase 1	KRAS G12C mutant Colorectal Cancer Second line KRAS G12C	20	Sotorasib 960 mg + Panitumumab 6 mg/kg	txtzrjpdts(wgsllkjjkj) = fvguzdqsos xxvegwcutd (kvztwnknul ) View more	Positive	18 Jan 2024
NCT03600883 (CodeBreaK 100, Pubmed)	Phase 1/2	KRAS G12C mutant Non-small Cell Lung Cancer KRAS G12C mutation \| PD-L1	174	Sotorasib	kiwrlwrynd(zfopuufsca) = The most common side effects included diarrhea pqswabthos (oytsidwtnw ) View more	-	01 Jan 2024
NCT04185883 (CodeBreaK 101, Pubmed \| Nat Med)	Phase 1	Advanced Malignant Solid Neoplasm Third line APC \| TP53 \| SMAD4 ... View more	-	Sotorasib	actqxjkhuk(gghkcynkjh) = ahegzamrtf xatdhxygqy (yjdvzuicis, 12.5 - notestimable)	Positive	01 Jan 2024
NCT05327491 (CTgov)	Phase 1	-	146	sotorasib (Treatment A)	ajwihjpcuc(ldwarygsaq) = uwqqfmdrvo qixhjvhgfc (jbjjyttlsk, rvoknnxkjk - dsfnsgaoez) View more	-	14 Dec 2023
NCT05327491 (CTgov)	Phase 1	-	146	sotorasib (Treatment B)	ajwihjpcuc(ldwarygsaq) = rzdnnkopra qixhjvhgfc (jbjjyttlsk, prhhbqspvj - xokfluilli) View more	-	14 Dec 2023

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