AXL inhibitors(AXL receptor tyrosine kinase inhibitors), RET inhibitors(Tyrosine-protein kinase receptor RET inhibitors), Tie-2 antagonists(TEK receptor tyrosine kinase antagonists)

Therapeutic Areas

NeoplasmsRespiratory DiseasesDigestive System Disorders+ [3]

Active Indication

NeoplasmsAdvanced Lung Non-Small Cell Squamous CarcinomaMetastatic Non-Squamous Non-Small Cell Lung Carcinoma+ [5]

Inactive Indication

Advanced cancerAdvanced LiposarcomaAdvanced Malignant Solid Neoplasm+ [21]

Originator Organization

Mirati Therapeutics, Inc.

Active Organization

Mirati Therapeutics, Inc.

BeOne Medicines Ltd.

BeiGene Pharmaceuticals (Guangzhou) Co. Ltd.

Inactive Organization

BeOne Pharmaceutical (Suzhou) Co. Ltd.

License Organization

BeOne Medicines Ltd.

Mirati Therapeutics, Inc.

Bristol Myers Squibb Co.

Drug Highest PhasePhase 3

First Approval Date-

Regulation-

Structure/Sequence

Molecular FormulaC33H29F2N5O4S

InChIKeyWLAVZAAODLTUSW-UHFFFAOYSA-N

CAS Registry1123837-84-2

Clinical Trials associated with Sitravatinib

NCT05564338

/ WithdrawnPhase 3

A Randomized, Double-blind, Placebo-controlled Phase 3 Study to Compare the Efficacy and Safety of Sitravatinib Plus Tislelizumab or Placebo Plus Tislelizumab Versus Placebo as Adjuvant Treatment in Patients With Hepatocellular Carcinoma Who Are at High Risk of Recurrence After Surgical Resection

The purpose of this study is to compare the efficacy and safety of sitravatinib plus tislelizumab or placebo plus tislelizumab versus placebo. The study will also compare the recurrence-free survival (RFS) in participants with hepatocellular carcinoma (HCC) who are at high risk of recurrence after surgical resection.

Start Date30 Jun 2023

Sponsor / Collaborator

BeOne Medicines Ltd.

NCT05614453

/ WithdrawnPhase 2

A Phase II Trial of Tislelizumab in Combination With Sitravatinib for Recurrent/Metastatic Cervical Cancer After Platinum-Based Chemotherapy

The goal of this clinical trial is to learn about the effect of the combination treatment of sitravatinib with tislelizumab in patients with Recurrent/Metastatic Cervical Cancer after Platinum-Based Chemotherapy.
The main question it aims to answer is the percentage of people in the study who have a partial or complete response to the treatment.
Participants will receive treatment under the care of their treating physician and will be reviewed regularly.

Start Date01 Jun 2023

Sponsor / Collaborator

Australia New Zealand Gynaecological Oncology Group

[+1]

ChiCTR2200065547

/ Not yet recruitingPhase 2IIT

A phase II, open-label, single-arm, multi-center, prospective clinical study to investigate the efficacy and safety of tislelizumab combined with sitravatinib and docetaxel in patients with locally advanced or metastatic non-small cell lung cancer that progressed on or after chemotherapy and anti-PD-(L)1 antibody

Start Date25 Nov 2022

Sponsor / Collaborator-

100 Clinical Results associated with Sitravatinib

100 Translational Medicine associated with Sitravatinib

100 Patents (Medical) associated with Sitravatinib

Literatures (Medical) associated with Sitravatinib

01 Apr 2026·INTERNATIONAL JOURNAL OF CANCER

Tislelizumab plus sitravatinib or anlotinib as maintenance therapy in extensive‐stage small‐cell lung cancer: Results of two prospective phase II studies

Article

Author: Lou, Guangyuan ; Chen, Kaiyan ; Li, Hui ; Lu, Hongyang ; Xie, Fajun ; Yu, Sizhe ; Xu, Yanjun ; Xu, Xiaoling ; Yu, Xinmin ; Gu, Cuiping ; Gong, Lei ; Qin, Jing ; Wang, Wenxian ; Zhao, Jun ; Han, Na ; Fan, Yun ; Huang, Zhiyu ; Shao, Lan

Abstract:

First‐line chemo‐immunotherapy has significantly improved survival in extensive‐stage small‐cell lung cancer (ES‐SCLC). However, rapid disease progression still occurs, with a median progression‐free survival (PFS) of only 4.5–5.8 months from induction therapy. We initiated two single‐arm, phase II studies to assess the first‐line maintenance therapy with tislelizumab plus anti‐angiogenic drugs following induction therapy in ES‐SCLC patients. Previously untreated ES‐SCLC patients were enrolled to receive tislelizumab plus platinum‐based chemotherapy as induction therapy for 4 cycles, followed by tislelizumab plus sitravatinib (Trial 1) or anlotinib (Trial 2) as maintenance therapy in a 21‐day cycle. The primary endpoint was the 1‐year PFS rate in the maintenance analysis set (MAS, including patients receiving ≥1 dose of maintenance therapy). Outcomes in MAS were calculated from the start of maintenance therapy. Twenty‐one patients were enrolled, and 18 patients entered the maintenance phase in each trial. From the start of the maintenance therapy, the median PFS was 6.4 and 7.8 months (1‐year PFS rates of 22.2% and not reached), respectively; the median overall survival (OS) was 18.3 months and not reached. From induction therapy, the corresponding median PFS was 9.1 and 10.8 months, with a median OS of 17.6 months and not reached. In MAS, the most common grade ≥3 treatment‐related adverse events (TRAEs) included hypertension (22.2%) in Trial 1 and fatigue (5.6%) in Trial 2. No patients died from TRAEs in either trial. Maintenance therapy with tislelizumab plus sitravatinib or anlotinib yielded clinically meaningful survival results and was generally well tolerated in ES‐SCLC, warranting further exploration in larger‐scale trials.

01 Apr 2026·JOURNAL OF HEPATOLOGY

Open-label, single-arm, phase II trial to investigate the efficacy of sitravatinib plus tislelizumab combination as a second-line treatment for advanced biliary tract cancer

Article

Author: Kang, Beodeul ; Chon, Hong Jae ; Kim, Jin Won ; Oh, Do-Youn ; Yoon, Jeesun ; Choi, Hye Jin ; Kim, Ji-Won ; Lee, Choong-Kun ; Park, Se Jun ; Kim, Tae-Yong ; Lee, Myung Ah

BACKGROUND & AIMS:

Immune checkpoint inhibitors (ICIs) combined with cytotoxic chemotherapy are now the standard first-line treatment for advanced biliary tract cancer (BTC). With this evolving landscape, therapeutic options using ICIs after first-line failure are urgently needed. Anti-angiogenic agents may enhance anti-tumor immunity by increasing tumor antigen presentation and promoting lymphocyte infiltration and migration. We aimed to evaluate the efficacy of sitravatinib plus tislelizumab as second-line therapy for advanced BTC.

METHODS:

In this open-label, single-arm, phase II trial, patients were enrolled regardless of prior ICI treatment history. The primary endpoint was disease control rate. Key secondary endpoints included objective response rate, progression-free survival, overall survival, safety, and biomarker analyses (NCT04727996).

RESULTS:

A total of 43 patients were enrolled. The median follow-up was 10.5 months (95% CI 7.03-15.6). Nine patients had previously received ICI therapy. The disease control rate was 65.1% (95% CI 50.3-78.0), and the objective response rate was 18.6% (95% CI 9.2-32.1). Median progression-free and overall survival were 4.93 months (95% CI 3.10-8.87) and 10.3 months (95% CI 6.67-18.2), respectively. Anti-tumor activity was observed regardless of prior ICI exposure. The most common treatment-related adverse events were associated with sitravatinib and were predominantly grade 1-2. In exploratory analyses, patients with homologous recombination deficiency (HRD), detected by baseline tissue next-generation sequencing (frequency 18.5%), showed better outcomes than those without HRD. Responders displayed higher inflammatory signaling in baseline and on-treatment tumor tissue compared with non-responders.

CONCLUSIONS:

Sitravatinib plus tislelizumab demonstrated meaningful efficacy and an acceptable safety profile as second-line therapy for advanced BTC. HRD-based patient selection may provide a promising strategy for optimizing treatment in this setting.

CLINICALTRIALS:

gov Identifier NCT04727996.

GOV IDENTIFIER:

NCT04727996 IMPACT AND IMPLICATIONS: The results of this multi-center, open-label, phase II study suggest that immunotherapy and anti-angiogenic agent combination treatment has a promising efficacy and safety as second-line treatment for patients with advanced biliary tract cancer. Furthermore, the presence of homologous recombination deficiency detected on tumor next-generation sequencing may select patients who have benefit from this combination, which supports further research exploring immunotherapy with anti-angiogenics combination strategy in this setting.

28 Feb 2026·RAPID COMMUNICATIONS IN MASS SPECTROMETRY

Metabolic Profiling of Sitravatinib in Rat and Human Liver Microsomes Using LC–MS/MS and LC–Orbitrap–HRMS

Article

Author: Xu, Shan ; Bao, Guanging ; Zhu, Ying ; Liu, Wenxia ; Li, Linfei

ABSTRACT:

Rationale:

Sitravatinib is a receptor tyrosine kinase inhibitor that has been developed for the treatment of advanced nonsmall‐cell lung cancer (NSCLC) and urothelial carcinoma. This study aimed at developing an integrated LC–MS/MS and LC–Orbitrap–HRMS platform for evaluating the metabolic stability and profiling the metabolites in rat and human liver microsomes.

Method:

Separation was achieved using a Waters ACQUITY BEH C 18 column with a gradient of 0.1% formic acid in water and acetonitrile. Detection utilized positive electrospray ionization and multiple reaction monitoring of transitions m/z 630.2 → 555.2 for sitravatinib and m/z 502.5 → 323.2 for the internal standard. Metabolite identification was performed using LC–Orbitrap–HRMS through full‐scan MS/dd‐MS 2 and parallel reaction monitoring. The structures of the metabolites were characterized via accurate mass measurement and MS 2 fragmentation interpretation.

Results:

The LC–MS/MS method showed excellent linearity over a concentration range of 1.0–2000 nM, suitable for high‐throughput in vitro assays. Sitravatinib demonstrated poor metabolic stability ( t1/2 = 17.47 ± 2.57 min) in rat liver microsomes, with seven metabolites identified. Among these, M3 and M5 were the major metabolites. In contrast, sitravatinib exhibited high metabolic stability in human liver microsomes ( t1/2 = 96.06 ± 12.17 min), with only seven minor metabolites detected.

Conclusions:

Key metabolic pathways included O ‐demethylation, amide formation, N ‐dealkylation, and oxidative deamination. This study establishes the first integrated LC–MS/MS and HRMS strategy for in vitro metabolic profiling of sitravatinib.

News (Medical) associated with Sitravatinib

04 Jun 2025

·www.prnewswire.com

2025 ASCO Oral Presentation: Innovent Biologics Announces Updated Data of IBI363 (First-in-class PD-1/IL-2α-bias Bispecific Antibody Fusion Protein) from the Phase 1 PoC Clinical Study in Advanced Non-small Cell Lung Cancer

SAN FRANCISCO and SUZHOU, China, June 3, 2025 /PRNewswire/ -- Innovent Biologics, Inc. ("Innovent") (HKEX: 01801), a world-class biopharmaceutical company that develops, manufactures and commercializes high-quality medicines for the treatment of oncology, autoimmune, cardiovascular and metabolic, ophthalmology and other major diseases, announced the third oral presentation of clinical data for IBI363 (first-in-class PD-1/IL-2α-bias bispecific antibody fusion protein) in advanced non-small cell lung cancer at the 2025 American Society of Clinical Oncology (ASCO), following IBI363's other two oral presentations in colorectal cancer and melanoma. A manageable safety profile, encouraging efficacy, and trends in long-term survival benefits have been observed in both immunotherapy-resistant squamous non-small cell lung cancer (NSCLC) and wild-type lung adenocarcinoma. It is worth mentioning that Innovent's pipeline has a total of 8 oral presentations at this ASCO conference, representing approximately 2% of the conference's total oral presentations. Innovent Biologics is conducting clinical studies in China, the United States, and Australia to explore the efficacy and safety of IBI363 for multiple tumor indications, including immune resistance, cold tumors, and front-line treatments. At this year's ASCO meeting, three oral presentations of IBI363 reported encouraging Phase 1/2 clinical data in the first three indications explored—NSCLC, CRC, and melanoma—focusing on IO-resistant and cold tumors. The data comprehensively demonstrated the breakthrough clinical outcomes of IBI363 across these indications, from robust tumor response to long-term survival benefits. These findings provide strong support of the drug's novel mechanism of action translating effectively into clinical outcomes, and imply its potential for broader clinical development, offering new hope in areas of immunotherapy where treatment options remain limited. PD-1/IL-2α-bias bispecific antibody fusion protein IBI363 in patients with immunotherapy resistant advanced non-small cell lung cancer: results from a Phase 1 study Updated data on IBI363 monotherapy in patients with advanced NSCLC were reported (ClinicalTrials.gov, NCT05460767). As of the data cutoff date, April 7, 2025, a total of 136 patients with NSCLC had received IBI363 monotherapy (2 μg/kg QW~4mg/kg Q3W), including 67 with squamous cell carcinoma and 58 with EGFR wild-type adenocarcinoma. IBI363 showed breakthrough therapeutic potential from tumor response to long-term survival benefit in immuno-resistant squamous NSCLC All 67 squamous NSCLC patients were EGFR wild type. Among them, 28 patients received IBI363 at 1 mg/kg Q2W or 1.5 mg/kg Q3W, and 31 patients received IBI363 at 3 mg/kg Q3W. In the two groups of patients, the proportion of ≥2 lines of previous systemic therapy was 64.3% (18/28) vs 67.7% (21/31), the proportion of previous anti-PD-1/PD-L1 therapy was 100% (28/28) vs 96.8% (30/31) and the proportion of PD-L1 TPS<1% was 35.7% (10/28) vs 41.9% (13/31). In the 1/1.5 mg/kg dose group, promising ORR/DCR/PFS/OS were observed. Median OS achieved 15.3 months, suggesting the potential long-term survival benefit of IBI363 as a PD-1/IL-2α-bias bispecific immunotherapy. Compared with the 1/1.5 mg/kg dose group, the 3 mg/kg Q3W dose group observed more prominent confirmed ORR (36.7%), DCR (90.0%), PFS (median PFS 9.3 months) and OS trends (median OS not reached, 12-month OS rate 70.9%) (see the table below). Among the patients with PD-L1 TPS<1%, IBI363 demonstrated outstanding efficacy signals: in the 1/1.5 mg/kg group (N=10), the confirmed ORR was 30.0% and the DCR was 90.0%, while that of the 3 mg/kg group (N=13) were 46.2% and 92.3%, suggesting the potential advantage of IBI363 in the population with low expression of PD-L1. IBI363 showed potential for long-term survival benefits in immuno-resistant wild-type lung adenocarcinoma, especially in patients with smoking history Among the 58 patients with EGFR wild-type lung adenocarcinoma, 30 patients received IBI363 at 0.6 mg/kg Q2W or 1 mg/kg Q2W or 1.5 mg/kg Q3W, 25 patients received IBI363 at 3 mg/kg Q3W. In the two groups of patients, the proportions of ≥2 lines of previous systemic therapy were 80.0% (24/30) vs 64.0% (16/25), the proportions of previous anti-PD-1/PD-L1 therapy were both 100%, the proportions of PD-L1 TPS<1% were 26.7% (8/30) vs 40.0% (10/25) and the proportions of smoking history were 56.7% (17/30) vs 60.0% (15/25). In the 1/1.5 mg/kg dose group, median OS achieved 17.5 months, suggesting the potential long-term survival benefit of IBI363 as a PD-1/IL-2α-bias bispecific immunotherapy. Compared with the 0.6/1/1.5 mg/kg dose group, the 3 mg/kg dose group observed higher confirmed ORR (24.0%), DCR (76.0%), PFS (median PFS 5.6 months) and OS trends (median OS not reached, 12-month OS rate 71.6%) (see the table below). Higher ORR and PFS were observed in lung adenocarcinoma patients with a history of smoking. Among them, the confirmed ORR in the 0.6/1/1.5 mg/kg group (N=17) was 23.5%, and the confirmed ORR in the 3 mg/kg group (N=15) was 33.3%. In all dose groups (N=32), the median PFS of smokers was longer than non-smokers: 5.3 (2.0, 7.0) vs 3.0 (1.6, 5.1) months. In terms of long-term survival benefits, after follow-ups of 12.0 and 13.7 months, the median OS for non-smokers was 13.6 months, whereas the median OS for smokers was not yet reached, with only 9 (28.1%) events occurring. IBI363 had a manageable safety profile in advanced NSCLC Among the 57 patients with NSCLC in the 3 mg/kg dose group, the most common treatment related adverse events (TRAEs) of grade 3 or above were arthralgia and rash. 7.0% of patients experienced TRAEs leading to discontinuation. The overall safety profile was manageable. In view of the encouraging efficacy signals and manageable safety demonstrated by IBI363 monotherapy, Innovent plans to conduct a Phase 3 registration clinical study in locally advanced or metastatic squamous NSCLC that has failed platinum-based chemotherapy and anti-PD-1 /PD-L1 immunotherapy. As of now, IBI363 has received Breakthrough Therapy (BTD) certification from China CDE and Fast Track Designation (FTD) from the US FDA for squamous NSCLC. Professor Jianya Zhou, The First Affiliated Hospital, School of Medicine, Zhejiang University, stated: "Lung cancer is the malignant tumor with the highest incidence and mortality rate both globally and in China[1], and it is a major issue endangering public health. Although immunotherapy has completely transformed the treatment landscape of NSCLC, for patients with wild-type NSCLC who have failed immunotherapy, the current standard treatment regimen docetaxel has limited efficacy, with an ORR of less than 20%, a PFS of less than 4 months, and an OS of less than 12 months [2-7]. In recent years, although the exploration of new treatment regimens such as immune combination therapy and antibody drug conjugates (ADCs) has brought new hope, many large-scale Phase 3 clinical studies on NSCLC patients who have failed platinum-based chemotherapy and immunotherapy have not achieved satisfactory results, and most of these studies have not met the primary endpoints[2-6]. Although the TROPION-Lung01 study achieved the primary endpoint of PFS in NSCLC, it did not reach the primary endpoint of OS. Especially in squamous NSCLC, no improvement was observed in PFS/OS/ORR in the experimental group. Therefore, there was a huge and urgent unmet medical need in NSCLC that has failed immunotherapy. As a PD-1/IL-2α-bias bispecific molecule, IBI363 not only shows clinical benefits in both ORR and PFS in immune-resistant NSCLC, but also enables us to see the potential of the tailing effect of immunotherapy to bring long-term survival benefits to patients compared with chemotherapy. We are also more looking forward to the survival data of the long-term follow up in the high dose IBI363 group." Dr. Hui Zhou, Senior Vice President of Innovent, stated: "It is a great pleasure to orally present the latest progress of IBI363 in the field of lung cancer at the ASCO conference. IBI363 shows remarkable efficacy in immune-resistant wild-type nsclc and clinical data suggests better trends in ORR, DCR, PFS and OS at higher doses. We expect longer-term follow-up to bring more mature data and look forward to seeing its potential as an immunotherapy for the long-term survival benefits of patients. Meanwhile, regardless of the expression level of PD-L1, IBI363 has demonstrated a powerful anti-tumor effect in immune-resistant NSCLC (especially squamous NSCLC), suggesting that the effect of IBI363 does not depend on the expression of PD-L1. In the future, it may also bring breakthroughs in cold tumors with low or no expression of PD-L1. We will continue to advance the clinical exploration of IBI363 in NSCLC and other tumor types." About IBI363 (First-in-class PD-1/IL-2α-bias bispecific antibody fusion protein) IBI363 is a first-in-class PD-1/IL-2α-bias bispecific antibody fusion protein independently developed by Innovent Biologics. It functions by both blocking the PD-1/PD-L1 pathway and activating the IL-2 pathway. The IL-2 arm of IBI363 is designed to maintain its affinity for IL-2Rα while reducing binding to IL-2Rβ and IL-2Rγ, thereby minimizing toxicity. The PD-1 binding arm not only blocks PD-1 but also selectively delivers IL-2. This approach targets and activates tumor-specific T cells that express both PD-1 and IL-2α, leading to more precise and effective activation of this T cell subpopulation. IBI363 has demonstrated robust antitumor activity in various tumor-bearing pharmacological models, but also showed outstanding efficacy in PD-1 resistance and metastasis models. In response to urgent clinical needs, Innovent is conducting clinical studies in China, the United States and Australia to further explore the efficacy and safety of IBI363 in various tumor indications, including immune-resistant, cold tumors, and front-line treatments. The first pivotal trial of IBI363 was initiated in 2025 for unresectable locally advanced or metastatic mucosal or acral melanoma who have not received prior systemic therapy. IBI363 has received two fast track designations (FTD) from the U.S. FDA and two breakthrough designations (BTD) from the China NMPA, for the treatment of squamous non-small cell lung cancer and melanoma, respectively. About Innovent Innovent is a leading biopharmaceutical company founded in 2011 with the mission to empower patients worldwide with affordable, high-quality biopharmaceuticals. The company discovers, develops, manufactures and commercializes innovative medicines that target some of the most intractable diseases. Its pioneering therapies treat cancer, cardiovascular and metabolic, autoimmune and eye diseases. Innovent has launched 15 products in the market. It has 3 new drug applications under regulatory review, 4 assets in Phase III or pivotal clinical trials and 15 more molecules in early clinical stage. Innovent partners with over 30 global healthcare companies, including Eli Lilly, Sanofi, Incyte, Adimab, LG Chem and MD Anderson Cancer Center. Guided by the motto, "Start with Integrity, Succeed through Action," Innovent maintains the highest standard of industry practices and works collaboratively to advance the biopharmaceutical industry so that first-rate pharmaceutical drugs can become widely accessible. For more information, visit , or follow Innovent on Facebook and LinkedIn. Forward-Looking Statements This news release may contain certain forward-looking statements that are, by their nature, subject to significant risks and uncertainties. The words "anticipate", "believe", "estimate", "expect", "intend" and similar expressions, as they relate to Innovent, are intended to identify certain of such forward-looking statements. Innovent does not intend to update these forward-looking statements regularly. These forward-looking statements are based on the existing beliefs, assumptions, expectations, estimates, projections and understandings of the management of Innovent with respect to future events at the time these statements are made. These statements are not a guarantee of future developments and are subject to risks, uncertainties and other factors, some of which are beyond Innovent's control and are difficult to predict. Consequently, actual results may differ materially from information contained in the forward-looking statements as a result of future changes or developments in our business, Innovent's competitive environment and political, economic, legal and social conditions. Innovent, the Directors and the employees of Innovent assume (a) no obligation to correct or update the forward-looking statements contained in this site; and (b) no liability in the event that any of the forward-looking statements does not materialize or turn out to be incorrect. References [1] Globocan 2022 (version 1.1) - 08.02.2024 [2] Paz-Ares LG, Juan-Vidal O, Mountzios GS, et al. Sacituzumab Govitecan Versus Docetaxel for Previously Treated Advanced or Metastatic Non-Small Cell Lung Cancer: The Randomized, Open-Label Phase III EVOKE-01 Study. J Clin Oncol. Aug 20 2024;42(24):2860-2872. doi:10.1200/JCO.24.00733 [3] Neal J, Pavlakis N, Kim SW, et al. CONTACT-01: A Randomized Phase III Trial of Atezolizumab + Cabozantinib Versus Docetaxel for Metastatic Non-Small Cell Lung Cancer After a Checkpoint Inhibitor and Chemotherapy. J Clin Oncol. Jul 10 2024;42(20):2393-2403. doi:10.1200/JCO.23.02166 [4] SAFFRON-301: Tislelizumab plus sitravatinib in advanced/metastatic NSCLC progressing on/after chemotherapy and anti–PD-(L)1. WCLC 2024. [5] 65O - Phase 3 LEAP-008 study of lenvatinib plus pembrolizumab versus docetaxel for metastatic non-small cell lung cancer (NSCLC) that progressed on a PD-(L)1 inhibitor and platinum-containing chemotherapy. ESMO IO 2023. [6] Canakinumab in combination with docetaxel compared with docetaxel alone for the treatment of advanced non-small cell lung cancer following platinum-based doublet chemotherapy and immunotherapy (CANOPY-2): A multicenter, randomized, double-blind, phase 3 trial. Lung Cancer . 2024 Mar:189:107451. doi: 10.1016/j.lungcan.2023.107451. Epub 2024 Jan 16. [7] Ahn MJ, Tanaka K, Paz-Ares L, et al. Datopotamab Deruxtecan Versus Docetaxel for Previously Treated Advanced or Metastatic Non-Small Cell Lung Cancer: The Randomized, Open-Label Phase III TROPION-Lung01 Study. J Clin Oncol. Sep 9 2024:JCO2401544. doi:10.1200/JCO-24-01544 SOURCE Innovent Biologics WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

Clinical ResultPhase 3Fast TrackPhase 1Immunotherapy

06 Nov 2023

·www.prnewswire.com

Mirati Therapeutics Reports Third Quarter 2023 Financial Results and Recent Corporate Updates

SAN DIEGO, Nov. 6, 2023 /PRNewswire/ -- Mirati Therapeutics, Inc.® (NASDAQ: MRTX), a commercial stage biotechnology company, today announced financial results for the third quarter 2023 along with recent pipeline and corporate updates. "We are pleased to share the significant progress made during the third quarter of 2023, highlighted by the advancement of our robust pipeline of targeted oncology programs and continued launch execution of KRAZATI®," said Charles Baum, M.D., Ph.D., CEO, president and founder, Mirati Therapeutics, Inc. "As we shared last month, we believe our pending acquisition by Bristol Myers Squibb will support the realization of the full potential of our therapies and enable the promise of a life beyond cancer. We look forward to continuing our work to improve the lives of people with cancer through Mirati discovered and developed therapeutics." Pipeline Updates Adagrasib (Potent and selective KRASG12C inhibitor) In November, the Company announced the United Kingdom Medicines and Healthcare Products Regulatory Agency (MHRA) granted conditional marketing authorization approval for KRAZATI (adagrasib) as a monotherapy indicated for the treatment of adult patients with advanced non-small cell lung cancer (NSCLC) with KRASG12C mutation and have progressive disease after prior therapy with, or intolerance to, platinum-based chemotherapy and/or anti-PD-1/PD-L1 immunotherapy. (View Release) In October, the Company shared updated results from the KRYSTAL-7 Phase 2 study evaluating adagrasib combined with pembrolizumab in patients with first-line NSCLC with a KRASG12C mutation at the European Society of Medical Oncology Congress (ESMO) 2023. (View Release) In September, the Company shared two-year follow-up data from a pooled analysis of the Phase 1/1b Cohort and Phase 2 Cohort A for the KRYSTAL-1 study evaluating adagrasib in NSCLC patients harboring a KRASG12C mutation at 2023 World Conference on Lung Cancer (WCLC). (View Release) In September, the Company shared that adagrasib has been included in the National Comprehensive Cancer Network (NCCN) Guidelines for Colon and Rectal Cancer for patients harboring a KRASG12C mutation. The Company completed enrollment in KRYSTAL-10, a Phase 3 registrational clinical study in second-line colorectal cancer patients with a KRASG12C mutation, evaluating the combination of adagrasib plus cetuximab versus chemotherapy. The Company continues to enroll in KRYSTAL-12, a Phase 3 clinical study of adagrasib versus docetaxel in second line NSCLC patients. Re-examination by the European Medicine Agency's (EMA) Committee for Medicinal Products for Human Use (CHMP) of the Conditional Marketing Authorisation Application (MAA) for KRAZATI (adagrasib) for the treatment of patients with KRASG12C-mutated advanced NSCLC is ongoing. MRTX1719 (MTA cooperative PRMT5 inhibitor) In August, the Company shared initial clinical data in patients with MTAP-deleted cancers. The Company continues to enroll patients in the Phase 1/2 clinical study. MRTX1133 (Potent and selective KRASG12D inhibitor) The Company continues to enroll patients in the Phase 1/2 clinical study. MRTX0902 (Potent SOS1 inhibitor) The Company continues to advance the Phase 1/2 clinical study evaluating the combination of MRTX0902 plus adagrasib. Recent Corporate Updates In October, the Company and Bristol Myers Squibb announced their entry into a merger agreement under which Bristol Myers Squibb has agreed to acquire Mirati for $58.00 per share in cash, for a total equity value of $4.8 billion. Mirati stockholders will also receive one non-tradeable Contingent Value Right (CVR) for each Mirati share held, potentially worth $12.00 per share in cash, representing an additional $1.0 billion of value opportunity. The transaction is anticipated to close by the first half of 2024, subject to fulfillment of customary closing conditions, including approval of the Company's stockholders and receipt of the required regulatory approvals. (View Release) In August, the Company executed an underwritten public offering. (View Release) Third Quarter Financial Results Cash, cash equivalents and short-term investments of approximately $976.4 million as of September 30, 2023, including proceeds from an August 2023 public offering of our common stock that generated net proceeds of $332.5 million. Excluding the August 2023 financing, net decrease in cash, cash equivalents and short-term investments for the third quarter of 2023 was $135.5 million. Net KRAZATI product revenue for the three and nine months ended September 30, 2023 was $16.4 million and $36.1 million, respectively. Net product revenue during the three and nine months ended September 30, 2023 is comprised of $15.1 million and $33.1 million, respectively, of commercial sales and $1.3 million and $3.0 million, respectively, of sales to a third-party commercial customer for its clinical trials. There was no product revenue for the same periods in 2022. License and collaboration revenue for the three and nine months ended September 30, 2023 was zero and $1.2 million, respectively, related to clinical supply revenue earned under the agreement with Zai Lab. License and collaboration revenue for the same periods in 2022 was $5.4 million and $11.5 million, respectively, related to milestone payments from Zai Lab and clinical supply revenue earned under the agreement with Zai Lab. Cost of product revenue for the three and nine months ended September 30, 2023 was $1.7 million and $3.8 million, respectively, of which $1.4 million and $3.0 million, respectively, related to product manufacturing and distribution costs, and royalties incurred on net sales of KRAZATI®. There was no cost of product revenue for the same periods in 2022. Research and development expenses for the three and nine months ended September 30, 2023 were $114.8 million and $365.6 million, respectively, compared to $131.1 million and $390.4 million for the same periods in 2022, respectively. The decrease was primarily driven by a reduction in clinical development costs for sitravatinib as the Company is no longer pursuing further clinical development, and a decrease in share-based compensation, partially offset by increases in costs for earlier stage clinical development programs such as MRTX1133. Selling, general and administrative expenses for the three and nine months ended September 30, 2023 were $72.0 million and $221.0 million, respectively, compared to $60.8 million and $169.0 million, respectively, for the same periods in 2022. The increases were primarily due to an increase in headcount-related costs, including share-based compensation, and commercial-related costs to support the marketing and sales of KRAZATI®. Net loss for the three months ended September 30, 2023 was $161.9 million, or $2.49 per share basic and diluted, compared to a net loss of $173.6 million, or $3.09 per share basic and diluted for the same period in 2022. Net loss for the nine months ended September 30, 2023 was $523.4 million, or $8.66 per share basic and diluted, compared to a net loss of $538.4 million, or $9.66 per share basic and diluted for the same period in 2022. About Mirati Therapeutics, Inc.® Mirati Therapeutics, Inc. is a commercial stage biotechnology company whose mission is to discover, design and deliver breakthrough therapies to transform the lives of patients with cancer and their loved ones. The company is relentlessly focused on bringing forward therapies that address areas of high unmet need, including lung cancer, and advancing a pipeline of novel therapeutics targeting the genetic and immunological drivers of cancer. Unified for patients, Mirati's vision is to unlock the science behind the promise of a life beyond cancer. For more information about Mirati, visit us at Mirati.com or follow us on Twitter, LinkedIn, and Facebook. Cautionary Statement Regarding Forward-Looking Statements This communication contains "forward-looking statements" within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended, regarding, among other things, Mirati Therapeutic, Inc.'s ("Mirati") business and financial guidance, the development and commercialization of certain biological compounds, including the therapeutic and commercial potential of KRAZATI® (adagrasib), sitravatinib (TAM receptor inhibitor), MRTX1719 (MTA-cooperative PRMT5 inhibitor), MRTX0902 (SOS1 inhibitor), and MRTX1133 (selective KRASG12D inhibitor), Mirati's other technologies and products in development, and the proposed acquisition of Mirati by Bristol-Myers Squibb Company ("BMS"). These statements may be identified by the fact they use words such as "should," "could," "expect," "anticipate," "estimate," "target," "may," "project," "guidance," "intend," "plan," "believe," "will" and other words and terms of similar meaning and expression in connection with any discussion of future operating or financial performance, although not all forward-looking statements contain such terms. All statements that are not statements of historical facts are, or may be deemed to be, forward-looking statements. These statements are only predictions, and such forward-looking statements are based on current expectations and involve inherent risks and uncertainties, including factors that could delay, divert or change any of them, and could cause actual outcomes and results to differ materially from current expectations. No forward-looking statement can be guaranteed. Actual results may differ materially from current expectations because of numerous risks and uncertainties including those inherent in the process of discovering, developing and commercializing medicines that are safe and effective for use as human therapeutics, those inherent in the endeavor of building a business around such medicines and those related to the proposed acquisition of Mirati by BMS, including with respect to (i) the approval of Mirati's stockholders for the proposed acquisition (which may be delayed or may not be obtained), (ii) whether the contingent consideration will become payable, (iii) the risk that the expected benefits or synergies of the acquisition will not be realized, (iv) the risk that legal proceedings may be instituted related to the merger agreement, (v) any competing offers or acquisition proposals for Mirati, (vi) the possibility that various conditions to the consummation of the acquisition may not be satisfied or waived, including that a governmental entity may prohibit, delay or refuse to grant approval for the acquisition, and (vii) unanticipated difficulties or expenditures relating to the proposed acquisition, the response of business partners and competitors to the announcement of the proposed acquisition and/or potential difficulties in employee retention as a result of the announcement and pendency of the proposed acquisition. The compounds described in this communication are subject to all the risks inherent in the drug development process, and there can be no assurance that the development of these compounds will be commercially successful. Forward-looking statements in this communication should be evaluated together with the many uncertainties that affect Mirati's business, particularly those identified in the cautionary factors discussion in Mirati's Annual Report on Form 10-K for the year ended December 31, 2022 (which is available at the Securities and Exchange Commission's (the "SEC") website ()), as well as other documents that may be filed by Mirati with the SEC from time to time. Mirati undertakes no obligation to publicly update any forward-looking statement, whether as a result of new information, future events or otherwise. The forward-looking statements made in this communication relate only to events as of the date on which the statements are made. Additional Information and Where to Find it In connection with the proposed acquisition of Mirati by BMS, Mirati filed a definitive proxy statement with the SEC on November 2, 2023. The definitive proxy statement and proxy card will be delivered to the stockholders of Mirati in advance of the special meeting relating to the proposed acquisition. This document is not a substitute for the proxy statement or any other document that may be filed by Mirati with the SEC. MIRATI'S STOCKHOLDERS AND INVESTORS ARE URGED TO READ THE DEFINITIVE PROXY STATEMENT IN ITS ENTIRETY AND ANY OTHER DOCUMENTS FILED WITH THE SEC IN CONNECTION WITH THE PROPOSED ACQUISITION OR INCORPORATED BY REFERENCE THEREIN BECAUSE THEY CONTAIN OR WILL CONTAIN, AS APPLICABLE, IMPORTANT INFORMATION ABOUT THE PROPOSED ACQUISITION AND THE PARTIES TO THE PROPOSED ACQUISITION. Investors and security holders can obtain a free copy of the definitive proxy statement, and will be able to obtain such other documents containing important information about Mirati once such documents are filed with the SEC, through the website maintained by the SEC at . Mirati makes available free of charge at its website at copies of materials it files with, or furnishes to, the SEC. Participants in the Solicitation This document does not constitute a solicitation of proxy, an offer to purchase or a solicitation of an offer to sell any securities. Mirati and its directors, executive officers and certain employees may be deemed to be participants in the solicitation of proxies from the stockholders of Mirati in connection with the proposed acquisition. Information regarding the identity of potential participants in the solicitation of proxies in connection with the proposed acquisition, and their direct or indirect interests, by security holdings or otherwise, is included in the definitive proxy statement relating to the proposed acquisition filed by Mirati with the SEC. To the extent holdings of Mirati's securities by its directors or executive officers have changed from the amounts set forth in the definitive proxy statement, such changes have been or will be reflected on Initial Statements of Beneficial Ownership on Form 3 or Statements of Beneficial Ownership on Form 4 filed with the SEC. These documents, when available, may be obtained free of charge from the SEC's website at and Mirati's website at . Mirati Contacts Investor Relations: [email protected] Media Relations: [email protected] SOURCE Mirati Therapeutics, Inc.

Phase 2ImmunotherapyDrug ApprovalPhase 3Acquisition

25 Oct 2023

·www.icr.ac.uk

Scientists discover new weakness in drug-resistant sarcomas, offering hope for smarter treatment strategies

In a major step forward for cancer research, scientists have uncovered a surprising vulnerability in soft tissue sarcomas – a rare and aggressive group of cancers that affect the soft tissues of the body, such as muscle, fat and blood vessels. The research team found that when these sarcomas acquire resistance to a commonly used class of drugs, they appear to become sensitive to another class of drugs to which they were previously resistant. This phenomenon, known as collateral sensitivity, could pave the way for smarter, more adaptive treatment strategies that anticipate and exploit the cancer’s next move. These findings will help inform sarcoma researchers around the world about potential resistance mechanisms that they can build upon in their research projects. The authors hope that, in the future, it will be possible to considerably improve patient outcomes by developing long-term treatment strategies that can provide therapeutic avenues to people with drug-resistant sarcomas. The findings of the study, which was led by researchers at The Institute of Cancer Research, London, have been published in the journal Communications Biology. The Institute of Cancer Research (ICR), which is both a research institute and a charity, helped fund the research, together with Sarcoma UK and the National Institute for Health Research Biomedical Research Centre at the ICR and The Royal Marsden NHS Foundation Trust. Soft tissue sarcomas are notoriously difficult to treat. Although multi-target tyrosine kinase inhibitors (mTKIs) – a class of drugs that block cancer-promoting proteins – have shown promise, their effectiveness is often short-lived. Most patients will find that their cancer develops resistance to mTKI treatment, and they are often left with limited therapy options afterwards. In certain types of soft tissue sarcoma and other types of cancer, clinicians have had success in treating patients with different single-target kinase inhibitors (sTKIs) one after the other. The idea behind this is that as the disease becomes resistant to one sTKI, the treatment is switched to an alternative sTKI that can target the cause of the resistance and help delay or stop the cancer from progressing. This process can then be repeated with more drugs as new resistance mechanisms arise. Sequential treatments with up to four of these drugs have helped improve patient outcomes in some cancers. Based on this, the team behind the current study decided to see whether sequential treatment with different mTKIs could overcome or delay the development of treatment resistance in soft tissue sarcomas. They selected four mTKIs – pazopanib, regorafenib, sitravatinib and anlotinib – that share some but not all kinase targets. Using laboratory models of soft tissue sarcoma, the researchers found that when the cancer became resistant to one of these drugs, the cells developed cross-resistance to the other ones too. In other words, switching from one mTKI to another would be unlikely to improve patient outcomes. However, the researchers realised that this resistance may come at a cost to the cancer itself. Unexpectedly, the resistant cells became newly vulnerable to drugs that target different pathways. For instance, cells that had developed resistance to sitravatinib developed sensitivity to infigratinib, which is a type of fibroblast growth factor receptor (FGFR) inhibitor. To explore this idea further, the researchers conducted a series of experiments to map out the genetic and molecular changes that were occurring. They found that resistant cells often undergo significant ‘rewiring’ of their signalling networks, altering the way they respond to external stimuli. These changes can create new dependencies – pathways that the cancer now relies on for survival – which it may be possible to target with precision therapies. The key to exploiting collateral sensitivity is to apply the concept of evolutionary steering. Rather than reacting to resistance after it occurs, scientists can aim to guide the cancer’s evolution in real time. By predicting which vulnerabilities will emerge and carefully sequencing appropriate treatments, they can, in theory, push cancer cells into states where they are more susceptible to other drugs. It is a strategy inspired by evolutionary game theory, where anticipating the next move of your opponent – in this case, cancer – can result in a win. To facilitate this, the research team hopes to develop diagnostic tools that can identify collateral sensitivities in individual patients. This would allow clinicians to create personalised treatment plans that adapt over time, using the cancer’s evolutionary trajectory as a guide. If, in the future, this treatment approach can be validated in human trials, it will have significant implications for clinical practice in soft tissue sarcomas and beyond. Joint first author Dr Andrew Jenks, Senior Scientific Officer in the Division of Cancer Biology at the ICR, said: “This is the first study to show that collateral sensitivity can be exploited in soft tissue sarcoma following the development of acquired resistance to mTKIs. The findings surprised us, as collateral sensitivity has not previously been observed in this setting. “Understanding the underlying mechanisms will allow for the creation of new treatment strategies designed to overcome drug resistance and provide more durable, longer-term therapeutic strategies for people living with soft tissue sarcoma.” Joint first author Dr Mark Elms, Scientific Officer at the ICR at the time of the study, said: “Our study reveals a promising therapeutic avenue in the fight against soft tissue sarcoma, a disease that has historically been very difficult to treat. By turning the cancer’s own resistance evolution against itself, we may be able to exploit collateral sensitivities and steer the cancer towards drug-sensitive states, thereby outsmarting the cancer by always staying one step ahead.” The team’s follow-up work will involve testing whether the same or similar drug resistance mechanisms are seen in tumour samples from soft tissue sarcoma patients. If this is the case, the researchers will aim to transfer their experiments to animal models. These are the first steps in translating the study findings into clinical settings. The researchers also plan to investigate whether similar patterns of resistance and sensitivity occur in other types of cancer. Senior author Professor Paul Huang, Group Leader of the Molecular and Systems Oncology Group at the ICR, said: “This study shows that although drug resistance closes some doors, it can open new ones. By understanding how treatment resistance evolves, we can begin to steer it in directions that make the cancer easier to treat. “Excitingly, this is just the beginning. We believe the principle of collateral sensitivity may apply much more broadly. If we can learn to predict and manipulate resistance, we could fundamentally change the way we treat multiple types of cancer.” Image credit: PIRO from Pixabay

100 Deals associated with Sitravatinib

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D11140	Sitravatinib	-	DB15036

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Indication	Highest Phase	Country/Location	Organization	Date
Hepatocellular Carcinoma	Phase 3	-	BeOne Medicines Ltd.	30 Jun 2023
Locally Advanced Lung Non-Small Cell Carcinoma	Phase 3	China	BeOne Medicines Ltd.	27 Jul 2021
Locally Advanced Lung Non-Small Cell Carcinoma	Phase 3	Australia	BeOne Medicines Ltd.	27 Jul 2021
metastatic non-small cell lung cancer	Phase 3	Australia	BeOne Pharmaceutical (Suzhou) Co. Ltd.	06 Jul 2021
Neoplasms	Phase 3	United States	BeOne Medicines Ltd.	19 Dec 2019
Neoplasms	Phase 3	China	BeOne Medicines Ltd.	19 Dec 2019
Neoplasms	Phase 3	Japan	BeOne Medicines Ltd.	19 Dec 2019
Neoplasms	Phase 3	Australia	BeOne Medicines Ltd.	19 Dec 2019
Neoplasms	Phase 3	France	BeOne Medicines Ltd.	19 Dec 2019
Neoplasms	Phase 3	Italy	BeOne Medicines Ltd.	19 Dec 2019

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04921358 (SAFFRON-301, Pubmed \| BMJ Oncol)	Phase 3	Locally Advanced Lung Non-Small Cell Carcinoma	377	Sitravatinib 100 mg + Tislelizumab 200 mg	wpopprkhec(elugihzxnj) = rmcrebalbc osaxjaphmp (eawldtulwu, 9.4 - 14.6) View more	Negative	01 Jan 2026
				Docetaxel 75 mg/m2	wpopprkhec(elugihzxnj) = hzxbckjdxg osaxjaphmp (eawldtulwu, 9.9 - 15.0) View more
NCT04727996 (Pubmed \| J Hepatol)	Phase 2	Advanced biliary tract cancer Second line	43	Sitravatinib plus tislelizumab	eetofwmxgz(mrerjqrwlu) = ktqheohjni ieigvgzrjw (daibkomjmf, 50.3 - 78.0) View more	Positive	01 Nov 2025
NCT04921358 (SAFFRON-301, CTgov)	Phase 3	Locally Advanced Lung Non-Small Cell Carcinoma	377	Tislelizumab+Sitravatinib (Tislelizumab + Sitravatinib)	itdyrettaq(ugsrnxipyn) = drsdqgniwp tmmhcrsrgl (vbffvftrlg, uhmnglkgew - umocqyiaqk) View more	-	29 Jun 2025
				Docetaxel (Docetaxel)	itdyrettaq(ugsrnxipyn) = klduxoafvh tmmhcrsrgl (vbffvftrlg, ynjchzquaz - vizfbnaxiu) View more
NCT05461794 (CTgov)	Phase 2	Metastatic Esophageal Squamous Cell Carcinoma	96	Tislelizumab+Sitravatinib (Arm A: Tislelizumab + Sitravatinib)	azmwghhjgh = gacdzvcrkb gwuvgexruy (vegaznhlau, aulzhhwbkb - mzgfenattw) View more	-	13 Jun 2025
				Docetaxel+Irinotecan (Arm C: Investigator-chosen Chemotherapy (ICC))	azmwghhjgh = iqqawtqhmx gwuvgexruy (vegaznhlau, qpznsgqelv - poaxyzqouk) View more
NCT04925986 (CTgov)	Phase 2	PD-L1 positive Non-squamous non-small cell lung cancer \| metastatic non-small cell lung cancer	9	Sitravatinib (Sitravatinib: Group 1A)	endkisfkzt(mtfifipvzd) = hvawbekaqw rsgmvxzwid (zrbmiuwtbr, bpazsfdnpq - jgqdrgiecp) View more	-	17 Apr 2025
				Sitravatinib (Sitravatinib: Group 2A)	endkisfkzt(mtfifipvzd) = hmuofymnjk rsgmvxzwid (zrbmiuwtbr, ogcodxkcol - noedgedbyo) View more
NCT04904302 (Pubmed \| Oncologist)	Phase 2	Metastatic Clear Cell Renal Cell Carcinoma	14	Sitravatinib + Nivolumab	pznaworswb(dookungbqn) = jlupxtrhle qrckwohhnw (xslvugqlpt ) View more	Positive	04 Apr 2025
				Prior Cabozantinib or Lenvatinib and ICI	yxfbytmhve(gmuhwiaiaw) = ytvxsncuth ytqbmurunt (uixjipfmax )
NCT02219711 (Phase Ib, Pubmed \| Future Oncol)	Phase 1	Solid tumor MET \| AXL \| RET ... View more	113	Sitravatinib	nplepmwkym(qmtainjuzl) = 61.1% lqmonohmcy (rytggpwfni ) View more	Positive	13 Dec 2024
NCT03941873 (BGB-900-104, CTgov)	Phase 1/2	Gastrooesophageal junction cancer \| Unresectable Hepatocellular Carcinoma	111	Sitravatinib (Sitravatinib Monotherapy: 80 mg)	ztedubszll = snvumecolw ulhacscvba (oisoexkjqi, aqgelnzcmm - ymnjsvpdzy) View more	-	18 Oct 2024
				Sitravatinib (Sitravatinib Monotherapy: 120 mg)	ztedubszll = falhiksaff ulhacscvba (oisoexkjqi, jcshyilrcu - uivbocnnma) View more
NCT05542342 (GEM-2101, ESMO2024) Manual	Phase 2	Uveal Melanoma Second line \| First line	16	Sitravatinibtislelizumab	fjyrugrxyr(qsxkhydqpz) = wlmiyrzcfu qfexelcdmk (fkcqlbfdrk ) View more	Positive	15 Sep 2024
NCT04921358 (SAFFRON-301, WCLC2024) Manual	Phase 3	Non-Small Cell Lung Cancer Second line \| Third line	377	Tislelizumab Sitravatinib	wzcnbqnotp(jrdmgiupce) = mdaiovmjxh tazvcmzdzs (rubfmekioj, 9.4 - 14.6) View more	Negative	08 Sep 2024
				docetaxelnib 100 mg	wzcnbqnotp(jrdmgiupce) = nkpcohrnzf tazvcmzdzs (rubfmekioj, 9.9 - 15.0) View more

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