On June 3, 2019 Bayer reported results of a new analysis from clinical trials investigating Vitrakvi (larotrectinib) in patients with TRK fusion cancer with primary central nervous system (CNS) tumors or brain metastases (Press release, Bayer, JUN 3, 2019, View Source [SID1234536847]). The analysis included 14 patients with primary CNS tumors evaluable for efficacy, including cases of glioma, glioblastoma, glioneural tumors, and astrocytoma. In this population, Vitrakvi demonstrated an overall response rate (ORR) of 36% (n=5; 95% CI: 13-65), including 14% complete responses (CR, n=2) and 21% partial responses (PR, n=3). The remaining 64% of patients had stable disease and no patients experienced progressive disease as best response based on investigator assessment using RANO (Response Assessment in Neuro-Oncology) and RECIST 1.1 (Response Evaluation Criteria In Solid Tumors). In five evaluable patients with NTRK gene fusion positive solid tumors with brain metastases, the ORR was 60% (n=3 PRs; 95% CI: 15-95) based on investigator assessment and RECIST 1.1. The remaining 40% of patients (n=2) had stable disease.1

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Vitrakvi is indicated for the treatment of adult and pediatric patients with solid tumors that have an NTRK gene fusion without a known acquired resistance mutation, are either metastatic or where surgical resection will likely result in severe morbidity, and have no satisfactory alternative treatments or that have progressed following treatment. This indication is approved under accelerated approval based on overall response rate and duration of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials.2

The analysis included 24 TRK fusion cancer patients with brain metastases or primary CNS tumors who were identified from across three different clinical studies.1 Eighteen patients presented with primary CNS tumors (data cut-off February 19, 2019), of which 14 were evaluable, and six patients had non-primary CNS tumors and brain metastases, of which five were evaluable (data cut-off July 30, 2018).1 The adverse events seen in the presentations were mostly grade 1-2.3,4,5

These data were presented in an oral presentation at ASCO (Free ASCO Whitepaper) on June 3, 2019 (Abstract 2006, Session: Central Nervous System Tumors; Monday, June 3, 3:15PM – 3:27PM CDT, Room: S102).

"These data are important as we continue to see efficacy with Vitrakvi in TRK fusion cancer across different tumor types and ages," said Scott Z. Fields, M.D., Senior Vice President and Head of Oncology Development at Bayer’s Pharmaceuticals Division. "The responses in these patients underscore the importance of widespread genomic cancer testing to identify patients who may be appropriate for this treatment."

Data on Vitrakvi in CNS tumors

A total of 24 patients with intracranial disease were identified from three clinical studies (adult Phase I trial, NCT02122913, 1 patient; Pediatric Phase I/II trial SCOUT, NCT02637687, 12 patients; and the adult/adolescent Phase II basket trial NAVIGATE, NCT02576431, 11 patients).1

About Vitrakvi (larotrectinib)
Vitrakvi is indicated for the treatment of adult and pediatric patients with solid tumors that have an NTRK gene fusion without a known acquired resistance mutation, are either metastatic or where surgical resection will likely result in severe morbidity, and have no satisfactory alternative treatments or that have progressed following treatment.2 This indication is approved under accelerated approval based on overall response rate and duration of response.2 Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials.2

Important Safety Information for VITRAKVI (larotrectinib)

Neurotoxicity: Among the 176 patients who received VITRAKVI, neurologic adverse reactions of any grade occurred in 53% of patients, including Grade 3 and Grade 4 neurologic adverse reactions in 6% and 0.6% of patients, respectively. The majority (65%) of neurologic adverse reactions occurred within the first three months of treatment (range 1 day to 2.2 years). Grade 3 neurologic adverse reactions included delirium (2%), dysarthria (1%), dizziness (1%), gait disturbance (1%), and paresthesia (1%). Grade 4 encephalopathy (0.6%) occurred in a single patient. Neurologic adverse reactions leading to dose modification included dizziness (3%), gait disturbance (1%), delirium (1%), memory impairment (1%), and tremor (1%).2

Advise patients and caretakers of these risks with VITRAKVI. Advise patients not to drive or operate hazardous machinery if they are experiencing neurologic adverse reactions. Withhold or permanently discontinue VITRAKVI based on the severity. If withheld, modify the VITRAKVI dose when resumed.2

Hepatotoxicity: Among the 176 patients who received VITRAKVI, increased transaminases of any grade occurred in 45%, including Grade 3 increased AST or ALT in 6% of patients. One patient (0.6%) experienced Grade 4 increased ALT. The median time to onset of increased AST was 2 months (range: 1 month to 2.6 years). The median time to onset of increased ALT was 2 months (range: 1 month to 1.1 years). Increased AST and ALT leading to dose modifications occurred in 4% and 6% of patients, respectively. Increased AST or ALT led to permanent discontinuation in 2% of patients.2

Monitor liver tests, including ALT and AST, every 2 weeks during the first month of treatment, then monthly thereafter, and as clinically indicated. Withhold or permanently discontinue VITRAKVI based on the severity. If withheld, modify the VITRAKVI dosage when resumed.2

Embryo-Fetal Toxicity: VITRAKVI can cause fetal harm when administered to a pregnant woman. Larotrectinib resulted in malformations in rats and rabbits at maternal exposures that were approximately 11- and 0.7-times, respectively, those observed at the clinical dose of 100 mg twice daily.2

Advise women of the potential risk to a fetus. Advise females of reproductive potential to use an effective method of contraception during treatment and for 1 week after the final dose of VITRAKVI.2

Most Common Adverse Reactions (≥20%): The most common adverse reactions (≥20%) were: increased ALT (45%), increased AST (45%), anemia (42%), fatigue (37%), nausea (29%), dizziness (28%), cough (26%), vomiting (26%), constipation (23%), and diarrhea (22%).2

Drug Interactions: Avoid coadministration of VITRAKVI with strong CYP3A4 inhibitors (including grapefruit or grapefruit juice), strong CYP3A4 inducers (including St. John’s wort), or sensitive CYP3A4 substrates. If coadministration of strong CYP3A4 inhibitors or inducers cannot be avoided, modify the VITRAKVI dose as recommended. If coadministration of sensitive CYP3A4 substrates cannot be avoided, monitor patients for increased adverse reactions of these drugs.2

Lactation: Advise women not to breastfeed during treatment with VITRAKVI and for 1 week after the final dose.2

Please see the full Prescribing Information for VITRAKVI (larotrectinib).

About TRK Fusion Cancer
TRK fusion cancer occurs when an NTRK gene fuses with another unrelated gene, producing an altered TRK protein.2 The altered protein, or TRK fusion protein, becomes constitutively active or overexpressed, triggering a signaling cascade.2 These TRK fusion proteins can act as an oncogenic driver, promoting cell proliferation and survival in tumor cell lines, leading to TRK fusion cancer, regardless of where it originates in the body.2 TRK fusion cancer is not limited to certain types of tissues and can occur in any part of the body.6 TRK fusion cancer occurs in various adult and pediatric solid tumors with varying frequency, including lung, thyroid, GI cancers (colon, cholangiocarcinoma, pancreatic and appendiceal), sarcoma, CNS cancers (glioma and glioblastoma), salivary gland cancers (mammary analogue secretory carcinoma) and pediatric cancers (infantile fibrosarcoma and soft tissue sarcoma).2,6

About Oncology at Bayer
Bayer is committed to delivering science for a better life by advancing a portfolio of innovative treatments. The oncology franchise at Bayer includes five marketed products and several other assets in various stages of clinical development. Together, these products reflect the company’s approach to research, which prioritizes targets and pathways with the potential to impact the way that cancer is treated.

On June 3, 2019 Aadi Bioscience, Inc. (Aadi), Aadi Bioscience, Inc (Aadi), a privately held clinical stage biopharmaceutical company, reported preliminary data on the ongoing nab-sirolimus (ABI-009) registration trial (AMPECT) for Advanced (metastatic or locally advanced) Malignant PEComa (perivascular epithelioid cell tumor) – a rare form of sarcoma for which there is no currently approved therapy (Press release, Aadi, JUN 3, 2019, View Source [SID1234536913]).

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Nanoparticle albumin-bound sirolimus (nab-Sirolimus), an mTOR inhibitor, received Breakthrough Therapy Designation from the US Food and Drug Administration (FDA) in Dec 2018, "for the treatment of patients with advanced (metastatic or locally advanced) malignant perivascular epithelioid cell tumor (PEComa)."

The AMPECT trial was conducted at 9 U.S. sites and enrolled 34 adult patients, with 31 confirmed as PEComa by a central pathology laboratory. PEComa origin sites in these patients included the uterus, pelvis, retroperitoneum, lung, kidney, liver, brain, muscle, ovary, aorta and small bowel.

These data, demonstrating a 42 percent confirmed investigator-assessed objective response rate (ORR) across advanced PEComas originating in various tissues, were released in an oral presentation at the American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) 2019 annual meeting in Chicago (abstract 11005). AMPECT Principal Investigator Andrew Wagner, M.D., Ph.D., from the Dana Farber Cancer Institute, said nab-sirolimus had delivered consistent and durable responses in advanced PEComa patients. "These responses were achieved with a manageable safety profile," Dr. Wagner said. "We saw a majority of the responding patients achieving a response by their first assessment at 6 weeks following initiation of therapy. Cytotoxic chemotherapies and other drugs approved for treatment of advanced sarcomas show only marginal benefit in PEComas. Activation of the mTOR pathway is common in PEComa and case reports have shown activity of mTOR inhibitors [1]. We are encouraged by the outcomes in this first-ever prospective clinical trial in advanced PEComa."

"The Aadi Bioscience team is proud to have contributed to this important study presented at ASCO (Free ASCO Whitepaper)," said Neil Desai, Ph.D., Chief Executive Officer of Aadi Bioscience. "We are grateful to the patients, families, and clinical trial teams who help push the boundaries of available care through their participation in clinical trials. These results are an important milestone in the ongoing development of nab-sirolimus across a wide range of diseases and therapeutic indications that are driven by mTOR activation and for which there is a need for new therapies." Dr. Desai added: "Results from the AMPECT study will serve as the basis for the ABI-009 New Drug Application (NDA) for nab-sirolimus, which the company expects to submit to the FDA in late 2019 or early 2020. The primary analysis for the NDA will rely upon central, independent radiology review, which will be performed in the second half of 2019. The company plans to release these data at a scientific meeting, which will also include additional patient follow-up, before the end of 2019."

Key Data Presented at ASCO (Free ASCO Whitepaper)

The primary efficacy outcome measure for the analysis presented at ASCO (Free ASCO Whitepaper) is investigator-assessed objective response rate (ORR) as measured by RECIST v 1.1. Key secondary endpoints include duration of response (DOR), progression-free survival (PFS), PFS rate at 6 months (PFS6) and safety. The data presented at ASCO (Free ASCO Whitepaper) employed a May 10, 2019 data cut-off, summarized below, was based on response assessments as performed by each respective clinical trial site (local, investigator-assessed radiology). A separate response assessment performed by independent radiologists, not yet completed, will be required to support global regulatory filings.

Consistent with agreements with the FDA, advanced PEComa patients enrolled in the Phase 2 trial (AMPECT) contributed to the efficacy analysis. The data presented are based on 34 patients evaluable for safety and 31 patients evaluable for efficacy per defined criteria in the protocol.

About Aadi Bioscience and nab-sirolimus (ABI-009)

Aadi is a clinical stage biopharmaceutical company led by Dr. Neil Desai, an inventor of ABRAXANE and the albumin-based technology platform. Aadi’s lead product nab-sirolimus (sirolimus albumin-bound nanoparticles for injectable suspension, ABI-009) is an mTOR inhibitor complexed with human albumin that has significantly higher tumor accumulation, mTOR target suppression and improved efficacy over other mTOR inhibitors in preclinical models. mTOR as a therapeutic target is well

On June 3, 2019 Xencor, Inc. (NASDAQ: XNCR), a clinical-stage biopharmaceutical company developing engineered monoclonal antibodies for the treatment of cancer, autoimmune diseases, asthma and allergic diseases, reported that the first patient has been dosed in a Phase 1 clinical study to evaluate the safety and tolerability of XmAb22841, both as a monotherapy and in combination with pembrolizumab, in patients with advanced solid tumors (Press release, Xencor, JUN 3, 2019, View Source [SID1234536793]). XmAb22841 is a bispecific antibody that simultaneously targets the immune checkpoint receptors CTLA-4 and LAG-3.

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"Our TME activators seek to improve the tolerability and clinical benefit of immunotherapy by activating T cells specifically in the tumor microenvironment, where many checkpoint receptors are highly expressed on immune cells. Toward that goal, XmAb22841 is designed with XmAb bispecific technology to target those cytotoxic T cells that simultaneously co-express the immune checkpoints CTLA-4 and LAG-3," said Paul Foster, M.D., senior vice president and chief medical officer at Xencor. "We intend to advance XmAb22841 in combination with anti-PD1 immunotherapy to potentially drive better responses through triple checkpoint blockade."

The Phase 1 dose-escalation and expansion study, which explores XmAb22841 as a monotherapy and in combination with pembrolizumab will characterize the safety and tolerability, pharmacokinetics, pharmacodynamics, immunogenicity and preliminary anti-tumor activity of intravenous administration in patients with select advanced solid tumors. For more information about the study, please visit View Source (identifier: NCT03849469).

About XmAb22841

XmAb22841 is a bispecific antibody that simultaneously targets immune checkpoint receptors CTLA-4 and LAG-3 and is designed to promote tumor-selective T-cell activation. Xencor’s XmAb bispecific Fc domain serves as the scaffold for these two antigen binding domains and confers long circulating half-life, stability and ease of manufacture. XmAb bispecific Fc domains have been engineered to eliminate Fc gamma receptor (FcγR) binding, with the intent to prevent activation and/or depletion of T cells via engagement by FcγR-expressing cells. XmAb22841 is being evaluated in a Phase 1 study for the treatment of advanced solid tumors, as a monotherapy and in combination with pembrolizumab.

On June 3, 2019 Oncopeptides AB (Nasdaq Stockholm: ONCO), a pharmaceutical company focused on the development of targeted therapies for difficult-to-treat hematological cancers, reported new data presented at the the 2019 American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Annual Meeting from its Phase 1/2 O-12-M1 clinical study of lead candidate melflufen (Press release, Oncopeptides, JUN 3, 2019, View Source [SID1234536810]). The data demonstrate that melflufen may offer positive disease stabilization and favorable time to next treatment (TTNT) outcomes in heavily-pretreated patients with relapsed/refractory multiple myeloma (RRMM).

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Overall conclusions from the data presented include:

Melflufen plus dexamethasone treatment results in disease stabilization in 76% of RRMM patients, which translates to a median TTNT of 7.9 months (10.6 months when censoring at time of death), which compares favorably with other relevant trials.
A median OS of 20.7 months in an advanced RRMM population, suggesting that melflufen therapy is associated with a long?term benefit and allows patients to receive further treatment to control disease.
Results support those of previous data showing the promising efficacy profile of melflufen for the treatment of RRMM.
The data is presented by Professor Paul G. Richardson, MD, RJ Corman Professor of Medicine at Harvard Medical School and Director of Clinical Research at the Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute, Boston, USA.

Oncopeptides recently announced that, following discussions with the U.S. Food & Drug Administration (FDA), the company has initiated the preparation for submitting a New Drug Application (NDA) for accelerated approval of melflufen for the treatment of patients with triple-class refractory multiple myeloma. The company targets to submit the application in the first quarter of 2020 based on the positive data from the ongoing Phase 2 HORIZON clinical trial.

"We are committed in helping patients with myeloma get access to melflufen given the safety and efficacy profile that is emerging from our clinical trials," said Jakob Lindberg, CEO of Oncopeptides. "In addition to the data presented at ASCO (Free ASCO Whitepaper), data from the melflufen clinical programs have also been selected for four presentations at the 2019 EHA (Free EHA Whitepaper) Annual Congress, including updated data from the HORIZON Phase 2 pivotal clinical trial that will serve as the foundation for our NDA submission."

The full poster presented at the 2019 ASCO (Free ASCO Whitepaper) Annual Meeting can be found on the company webpage under:

www.oncopeptides.com / Investors & Media / Presentations / 2019 ASCO (Free ASCO Whitepaper) Annual Meeting – poster

About the O-12-M1 Clinical Trial
O?12?M1 is a Phase 1/2 study with melflufen plus dexamethasone in 62 patients with RRMM who had ≥2 prior lines of therapy, prior exposure to at least an IMiD and a proteasome inhibitor, and disease progression on last line of therapy. Final study results were presented at the 2017 American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting.

Summary of O-12-M1 Data
At the time of data cutoff on November 9, 2017, 45 patients had been treated with 40 mg melflufen and dexamethosone. Median age was 66 years (47-78). 60% of patients were ISS stage II/III and 44% were high-risk cytogenetics. Patients had four median prior lines of therapy, with 91% of patients being single refractory, 67% of patients double refractory and 7% triple refractory. Further, 53% of patients were alkylator refractory. At data cutoff, 44 pts (98%) discontinued melflufen + dexamethasone, mainly due to adverse events (40%) and PD (31%). 27 patients received subsequent therapy. Median time from start of melflufen and dexamethasone to first subsequent therapy or death (TTNT), whichever occurred first, was 7.9 months (95% CI: 5.68-11.01). The majority of patients’ (52%) next therapy was single-agent with or without steroid therapy, and approximately half of patients receiving subsequent therapy (44%) received at least two subsequent lines of therapy.

Table: TTNT with Melflufen in O-12-M1 and Other Agents in RRMM

TTNT with Melflufen in O-12-M1

For further information, please contact:
Jakob Lindberg, CEO of Oncopeptides
E-mail: [email protected]
Telephone: +46 (0)8 615 20 40

Rein Piir, Head of Investor Relations at Oncopeptides
E-mail: [email protected]
Cell phone: +46 (0)70 853 72 92

This information was submitted for publication at 15.00 CET, June 3, 2019

About melflufen
Melflufen is a lipophilic peptide-conjugated alkylator that rapidly delivers a highly cytotoxic payload into myeloma cells through peptidase activity. It belongs to the novel class Peptidase Enhanced Cytotoxics (PEnC), which is a family of lipophilic peptides that exhibit increased activity via peptidase cleavage and have the potential to treat many cancers. Peptidases play a key role in protein homeostasis and feature in cellular processes such as cell-cycle progression and programmed cell death. Melflufen is rapidly taken up by myeloma cells due to its high lipophilicity and immediately cleaved by peptidases to deliver an entrapped hydrophilic alkylator payload. In vitro, melflufen is 50-fold more potent in myeloma cells than the alkylator payload itself due to the peptidase cleavage, and induces irreversible DNA damage and apoptosis. Melflufen displays cytotoxic activity against myeloma cell lines resistant to other treatments, including alkylators, and has also demonstrated inhibition of DNA repair induction and angiogenesis in preclinical studies.

On June 3, 2019 Merck, a leading science and technology company, reported updated results from the potentially registrational Phase II VISION study, showing durable anti-tumor clinical activity for the investigational targeted therapy tepotinib* across different lines of treatment in advanced non-small cell lung cancer (NSCLC) patients harboring MET exon 14 skipping mutations detected by liquid biopsy (LBx) or tissue biopsy (TBx) (Press release, Merck & Co, JUN 3, 2019, View Source [SID1234536831]). Data were shared in an oral presentation today at the 2019 American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Annual Meeting in Chicago, IL, US.

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"Tepotinib has been designed to potentially improve outcomes in aggressive tumors that have a poor prognosis and harbor these specific alterations," said Luciano Rossetti, Global Head of Research & Development for the Biopharma business of Merck. "Tepotinib is an important part of our strategic focus on precision medicine, and both the proportion of patients responding and the duration of anti-tumor clinical activity demonstrate the potential of this investigational therapy."

Discovered in-house at Merck, tepotinib is an investigational, highly potent and selective1 oral MET kinase inhibitor that is designed to inhibit the oncogenic signaling caused by MET (gene) alterations, including both MET exon 14 skipping mutations and MET amplifications, or MET protein overexpression. Alterations of the MET signaling pathway are found in various cancer types, including 3-5% of NSCLC cases, and correlate with aggressive tumor behavior and poor clinical prognosis.2-4

"Patients with this NSCLC molecular subtype lack treatment options that have the potential to significantly improve clinical outcomes," said Paul K. Paik, M.D., primary study investigator and Clinical Director, Thoracic Oncology Service, Memorial Sloan Kettering Cancer Center. "It is noteworthy to see data that are consistent with tepotinib’s previously reported efficacy findings in this patient population, and that also provide valuable new insight into its durable clinical activity across various treatment lines."

Results from the ongoing Phase II VISION study in 73 efficacy-evaluable patients with NSCLC with MET exon 14 skipping mutations identified by LBx or TBx demonstrate overall objective response rate (ORR) of 50.0% for LBx-identified patients as assessed by Independent Review Committee (IRC), and 55.3% as assessed by investigators. The ORR for TBx-identified patients was 45.1% and 54.9%, respectively. The overall median duration of response (DOR) was 12.4 months and 17.1 months among LBx-identified patients, as assessed by IRC and investigators, respectively, while among TBx-identified patients, 15.7 and 14.3 months were observed, respectively.

Most treatment-related adverse events (TRAEs) were Grade 1 and 2. No Grade 4 or 5 TRAEs were observed. Any grade TRAEs reported by ≥10% of 87 patients evaluable for safety were peripheral edema (48.3%), nausea (23.0%) diarrhea (20.7%) and increased blood creatinine (12.6%). Other relevant TRAEs of any grade include increased lipase (4.6%), fatigue (3.4%) and vomiting (3.4%). TRAEs led to permanent discontinuation in four patients (two patients due to peripheral edema, one due to interstitial lung disease, one due to diarrhea and nausea).

The use of both liquid and tissue biopsies to identify patients for the VISION trial is intended to support improved patient selection and is consistent with the company’s focus on patient-centric drug development.

Tepotinib is currently being investigated in NSCLC in two different settings: in NSCLC harboring MET alterations (MET exon 14 skipping mutations and MET amplifications) as monotherapy, as well as in combination with the tyrosine kinase inhibitor (TKI) osimertinib in epidermal growth factor receptor (EGFR) mutated MET amplified NSCLC having acquired resistance to prior EGFR TKI. Additional information on these clinical trials can be found at ClinicalTrials.gov using the identifiers NCT02864992 and NCT03940703, respectively. Merck is also actively assessing the potential of investigating tepotinib in combination with novel therapies for other tumor indications.

*Tepotinib is the recommended International Nonproprietary Name (INN) for the MET kinase inhibitor (MSC2156119J). Tepotinib is currently under clinical investigation and not approved for any use anywhere in the world.

Notes to Editors
Tepotinib oral session:

Title

Lead Author

Abstract #

Presentation
Date / Time
(CDT)

Location

Tepotinib

Oral Session

Phase II study of
tepotinib in
NSCLC patients with

METex14 mutations

P.K. Paik

9005

Mon, Jun 3, 8:00

AM – 11:00 AM
(9:24 AM – 9:36
AM lecture time)

Hall B1

About Non-Small Cell Lung Cancer
With 2 million cases diagnosed annually, lung cancer (including trachea, bronchus, and lung) is the most common type of cancer worldwide, and the leading cause of cancer-related death, with 1.7 million mortality cases worldwide.5 Alterations of the MET signaling pathway, including MET exon 14 skipping mutations and MET amplifications, occur in 3-5% of NSCLC cases.2-4

About Tepotinib
Tepotinib, discovered in-house at Merck, is an investigational oral MET inhibitor that is designed to inhibit the oncogenic MET receptor signaling caused by MET (gene) alterations, including both MET exon 14 skipping mutations and MET amplifications, or MET protein overexpression. It has been designed to have a highly selective mechanism of action, with the potential to improve outcomes in aggressive tumors that have a poor prognosis and harbor these specific alterations.

Tepotinib is currently being investigated in NSCLC and Merck is actively assessing the potential of investigating tepotinib in combination with novel therapies and in other tumor indications.

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