A Parallel Phase 2 Study of Glesatinib, Sitravatinib or Mocetinostat in Combination With Nivolumab in Advanced or Metastatic Non-Small Cell Lung Cancer

The study will evaluate the clinical activity of nivolumab in combination with 3 separate investigational agents, glesatinib, sitravatinib, or mocetinostat.

Start Date07 Nov 2016

Sponsor / Collaborator

Mirati Therapeutics, Inc.

NCT02544633 / CompletedPhase 2

Phase 2, Parallel-Arm Study of MGCD265 in Patients With Locally Advanced or Metastatic Non-Small Cell Lung Cancer With Activating Genetic Alterations in Mesenchymal-Epithelial Transition Factor

MGCD265 is an orally administered receptor tyrosine kinase inhibitor that targets MET and other receptors. This study is a Phase 2 trial of MGCD265 in patients with locally advanced, unresectable or metastatic non-small cell lung cancer (NSCLC) that has activating genetic changes of the MET gene (mutation or amplification [increase number of gene copies]). Testing for tumor gene changes can be performed in tumor tissue or blood samples. Patients must have previously received treatment with chemotherapy. The number of patients to be enrolled will depend on how many enrolled patients experience tumor size reduction. MGCD265 will be administered orally, twice daily. The study is designed to evaluate whether the number of patients experiencing tumor size reduction is substantially higher than would be expected with other available treatments.

Start Date01 Oct 2015

Sponsor / Collaborator

Mirati Therapeutics, Inc.

NCT01930006 / CompletedPhase 1

Phase 1 Single Dose 2-Way Crossover Comparative Bioavailability Study Of Two Oral Formulations Of MGCD265 In Healthy Male And Female Subjects - Fasting State

In this study two MGCD265 oral formulations at dose level of 100 mg are administered to healthy male and female subjects under fasting conditions.

Start Date01 Aug 2013

Sponsor / Collaborator

Mirati Therapeutics, Inc.

100 Clinical Results associated with Glesatinib

100 Translational Medicine associated with Glesatinib

100 Patents (Medical) associated with Glesatinib

Literatures (Medical) associated with Glesatinib

01 Jan 2023·Targeted oncology

Phase I Study Evaluating Glesatinib (MGCD265), An Inhibitor of MET and AXL, in Patients with Non-small Cell Lung Cancer and Other Advanced Solid Tumors

Article

Author: Bazhenova, Lyudmila ; Hurwitz, Herbert ; Reckamp, Karen L ; Sharma, Sunil ; Shapiro, Geoffrey I ; Christensen, James G ; Chao, Richard ; Cho, Byoung Chul ; Kollmannsberger, Christian ; Der-Torossian, Hirak ; Park, Keunchil ; Potvin, Diane ; Tassell, Vanessa ; Faltaos, Demiana ; Hong, David

BACKGROUND:

Heightened signaling by mesenchymal epithelial transition factor (MET) is implicated in tumorigenesis. Glesatinib is an investigational, oral inhibitor of MET and AXL.

OBJECTIVE:

This phase I study determined the maximum tolerated dose (MTD), recommended phase II dose (RP2D), and safety profile of glesatinib in patients with advanced or unresectable solid tumors. Antitumor activity and pharmacokinetics (PK) were secondary objectives.

PATIENTS AND METHODS:

Four formulations of glesatinib glycolate salt (capsule, unmicronized, micronized, and micronized version 2 [V2] tablets) and two free-base formulations (free-base suspension [FBS] capsule and spray-dried dispersion [SDD] tablet), developed to enhance drug exposure and optimize manufacturing processes, were evaluated in patients with genetically unselected advanced/unresectable solid tumors. MTD, based on dose-limiting toxicities (DLTs) observed during the first 21-day treatment cycle, was further evaluated in dose-expansion cohorts comprising patients with overexpression of MET and/or AXL, MET/AXL amplification, MET-activating mutations, or MET/AXL rearrangements for confirmation as the RP2D.

RESULTS:

Glesatinib was evaluated across 27 dose-escalation cohorts (n = 108). Due to suboptimal exposure with glesatinib glycolate salt formulations in the initial cohorts, investigations subsequently focused on the FBS capsule and SDD tablet; for these formulations, MTD was identified as 1050 mg twice daily and 750 mg twice daily, respectively. An additional 71 patients received glesatinib in the FBS and SDD dose-expansion cohorts. At MTDs, the most frequent treatment-related adverse events were diarrhea (FBS, 83.3%; SDD, 75.0%), nausea (57.1%, 30.6%), vomiting (45.2%, 25.0%), increased alanine aminotransferase (45.2%, 30.6%), and increased aspartate aminotransferase (47.6%, 27.8%). Exploratory pharmacodynamic analyses indicated target engagement and inhibition of MET by glesatinib. Antitumor activity was observed with glesatinib FBS 1050 mg twice daily and SDD 750 mg twice daily in tumors harboring MET/AXL alteration or aberrant protein expression, particularly in patients with non--small cell lung cancer (NSCLC). In patients with NSCLC, the objective response rate was 25.9% in those with MET/AXL mutation or amplification and 30.0% in a subset with MET-activating mutations. All six partial responses occurred in patients with tumors carrying MET exon 14 deletion mutations.

CONCLUSIONS:

The safety profile of single-agent glesatinib was acceptable. SDD 750 mg twice daily was selected as the preferred glesatinib formulation and dose based on clinical activity, safety, and PK data. Observations from this study led to initiation of a phase II study of glesatinib in patients with NSCLC stratified by type of MET alteration (NCT02544633).

CLINICAL TRIALS REGISTRATION:

ClinicalTrials.gov NCT00697632; June 2008.

31 Dec 2022·Cancer biology & therapyQ3 · MEDICINE

Functional proteomics of patient derived head and neck squamous cell carcinoma cells reveal novel applications of trametinib

Q3 · MEDICINE

Article

Author: Kulesz-Martin, Molly ; Clayburgh, Daniel ; Andersen, Peter ; McWeeney, Shannon ; Lucero, Olivia ; Mathieson, Chase ; Tyner, Jeffrey W. ; Jennings, Jennifer ; Vigoda, Myles ; Evans, Nathaniel ; Petrisor, Daniel ; Hale, Carolyn ; Jeng, Sophia ; Li, Ryan ; Bottomly, Daniel

In this study, we report a differential response of mitogen-activated protein kinase-kinase (MEK) inhibitor trametinib in 20 head and neck squamous cell carcinoma (HNSCC) patients' tumor-derived cell cultures. Relatively sensitive and resistant cases to trametinib were identified using high throughput metabolic assays and validated in extended dose response studies in vitro. High throughput metabolic assays exploring combination therapies with trametinib were subjected to synergy models and maximal synergistic dose analyses. These yielded several candidates, including axtinib, GDC-0032, GSK-690693, and SGX-523. The combination regimen of trametinib and AXL/MET/VEGFR inhibitor glesatinib showed initial efficacy both in vitro and in vivo (92% reduction in tumor volume). Sensitivity was validated in vivo in a patient-derived xenograft (PDX) model in which trametinib as a single agent effected reduction in tumor volume up to 72%. Reverse Phase Protein Arrays (RPPA) demonstrated differentially expressed proteins and phosphoproteins upon trametinib treatment. Furthermore, resistant cell lines showed a compensatory mechanism via increases in MAPK and non-MAPK pathway proteins that may represent targets for future combination regimens. Intrinsic-targeted options have potential to address paucity of medical treatment options for HNSCC cancer patients, enhance response to extrinsic targeted agents, and/or reduce morbidity as neoadjuvant to surgical treatments.

01 Mar 2022·Targeted oncologyQ3 · MEDICINE

Phase I Study of Glesatinib (MGCD265) in Combination with Erlotinib or Docetaxel in Patients with Advanced Solid Tumors

Q3 · MEDICINE

Article

Author: Der-Torossian, Hirak ; Chao, Richard ; Patnaik, Amita ; O'Dwyer, Peter J ; Potvin, Diane ; Gadgeel, Shirish ; Tassell, Vanessa ; Papadopoulos, Kyriakos P ; Haas, Naomi B ; Rasco, Drew W ; Faltaos, Demiana ; Tawashi, Manal

BACKGROUND:

Oncogenic drivers in solid tumors include aberrant activation of mesenchymal epithelial transition factor (MET) and AXL.

OBJECTIVE:

This study investigated the safety and antitumor activity of glesatinib, a multitargeted receptor tyrosine kinase inhibitor that inhibits MET and AXL at clinically relevant doses, in combination with erlotinib or docetaxel.

PATIENTS AND METHODS:

The phase I portion of this open-label, multicenter study included two parallel arms in which ascending doses of oral glesatinib (starting dose 96 mg/m²) were administered with erlotinib or docetaxel (starting doses 100 mg once daily and 50 mg/m², respectively) using a modified 3 + 3 design. Maximum tolerated dose (MTD) was based on dose-limiting toxicities (DLTs) during the first 21-day treatment cycle. Enrollment focused on patients with solid tumor types typically associated with MET aberration and/or AXL overexpression. The primary objective was to determine the safety profile of the treatment combinations. Antitumor activity and pharmacokinetics (PK) were also assessed.

RESULTS:

Ten dose levels of glesatinib across three glycolate formulations (unmicronized, micronized, or micronized version 2 [V2] tablets) available during the course of the study were investigated in 14 dose-escalation cohorts (n = 126). MTDs of unmicronized glesatinib plus erlotinib or docetaxel, and micronized glesatinib plus erlotinib were not reached. Micronized glesatinib 96 mg/m² plus docetaxel exceeded the MTD. Further dosing focused on glesatinib micronized V2: maximum administered dose (MAD) was 700 mg twice daily with erlotinib 150 mg once daily or docetaxel 75 mg/m² every 3 weeks. DLTs, acceptable at lower glesatinib (micronized V2) dose levels, occurred in two of five and two of six patients at the MADs of glesatinib + erlotinib and glesatinib + docetaxel, respectively. Across all cohorts, the most frequent treatment-related adverse events were diarrhea (glesatinib + erlotinib: 84.1%; glesatinib + docetaxel: 45.6%), fatigue (46.4%, 70.4%), and nausea (30.4%, 35.1%). The objective response rate was 1.8% and 12.0% in all glesatinib + erlotinib and glesatinib + docetaxel cohorts, respectively.

CONCLUSIONS:

The safety profile of glesatinib plus erlotinib or docetaxel was acceptable and there were no PK interactions. MADs of glesatinib 700 mg twice daily (micronized V2) with erlotinib 150 mg once daily or docetaxel 75 mg/m² every 3 weeks exceeded the MTD by a small margin. Modest signals of efficacy were observed with these treatment combinations in non-genetically selected patients with advanced solid tumors.

CLINICAL TRIALS REGISTRATION:

ClinicalTrials.gov NCT00975767; 11 September 2009.

News (Medical) associated with Glesatinib

08 Mar 2018

·www.biospace.com

Mirati Therapeutics Reports Fourth Quarter And Full-Year 2017 Financial Results

SAN DIEGO, March 8, 2018 /PRNewswire/ --Mirati Therapeutics Inc. (NASDAQ: MRTX), a clinical stage oncology biotechnology company, today reported financial results for the fourth quarter and full-year ended December 31, 2017. "We made significant progress in our key programs in 2017," said Charles M. Baum, M.D., Ph.D., President and Chief Executive Officer. "Promising data from the sitravatinib and KRAS programs encouraged us to pursue a more aggressive approach to accelerate development, supported by the successful financing we completed in November. In early 2018, we initiated a strategic regional partnership with BeiGene Ltd. that we anticipate will rapidly expand the development of sitravatinib in multiple tumor types. We expect to report multiple key catalysts in 2018, including a mid-year clinical update for our sitravatinib program. Our KRAS inhibitor program, an important yet elusive target, is growing and we remain on track for an IND filing in the fourth quarter of 2018." Recent Corporate Highlights Sitravatinib clinical data presented at 2017 IASLC World Conference on Lung Cancer Combination of sitravatinib and nivolumab in non-small cell lung cancer (NSCLC) patients with documented progression following checkpoint inhibitor therapy demonstrated 3 confirmed Partial Responses in first 11 evaluable patients First evaluable NSCLC patient with CBL inactivating mutation treated with single agent sitravatinib demonstrated confirmed Partial Response with 77% tumor reduction KRAS G12C lead candidates selected and advanced into IND-enabling development activities Significant achievement in development of a direct inhibitor of KRAS, a well-known but previously undruggable cancer mutation A potentially transformational, first-in-class treatment for 14% of NSCLC and 5% of colorectal cancer patients Program is on track to advance to IND filing in the fourth quarter of 2018 Exclusive license agreement initiated with BeiGene Ltd. for the development, manufacture and commercialization of sitravatinib in Asia (excluding Japan), Australia and New Zealand Expected to accelerate development of sitravatinib in NSCLC as well as other key indications including bladder, renal and hepatocellular cancer $86.7M public offering completed in November 2017; $150.8M of cash, cash equivalents and short-term investments as of December 31, 2017 Fourth Quarter and Full Year Financial Results Cash, cash equivalents, and short-term investments were $150.8 million on December 31, 2017, as compared to $56.7 million on December 31, 2016. Research and development expenses for the fourth quarter of 2017 were $15.2 million, compared to $16.0 million for the same period in 2016. Research and development expenses for the year ended December 31, 2017 were $58.1 million, compared to $68.5 million for the same period in 2016. The decrease in research and development expenses for both periods is primarily due to a reduction in glesatinib expenses and a reduction in share-based compensation expense. These decreases are partially offset by increases in expenses associated with our ongoing sitravatinib clinical trials. General and administrative expenses for the fourth quarter of 2017 were $3.0 million, compared to $3.9 million for the same period in 2016. General and administrative expenses for the year ended December 31, 2017 were $13.5 million, compared to $15.3 million for the same period in 2016. The decrease in general and administrative expense for both periods is primarily due to a decrease in share-based compensation expense. Net loss for the fourth quarter of 2017 was $17.9 million, or $0.67 per share basic and diluted, compared to net loss of $19.7 million, or $0.99 per share basic and diluted for the same period in 2016. Net loss for the year ended December 31, 2017 was $70.4 million, or $2.78 per share basic and diluted, compared to net loss of $83.1 million, or $4.20 per share basic and diluted for the same period in 2016.

Financial StatementFirst in ClassCollaborate

08 Apr 2013

·www.biospace.com

MethylGene Presents Preclinical Data on MG516 at the American Association for Cancer Research Annual Meeting

Montreal, Canada, April, 8, 2013 – MethylGene Inc. (TSX:MYG) today announced that preclinical data for the kinase inhibitor MG516 was presented at the American Association for Cancer Research (AACR) Annual Meeting held in Washington DC. In a poster entitled “Preclinical characterization of MG516, a novel inhibitor of receptor tyrosine kinases involved in resistance to targeted therapies” data was presented showing that MG516 possesses potent inhibitory activity against a spectrum of tyrosine kinase receptor targets including Eph receptors and Ret as well as Met, Axl and VEGF-R family members. The study incorporated data from in vitro kinase and cell-based analyses. In a broad variety of animal models of human cancer, MG516 demonstrated significant inhibition of tumor growth accompanied by suppression of the target kinases. MG516 also reversed resistance to the VEGFR inhibitor sunitinib in an in vivo preclinical tumor model. “MG516 inhibits a novel spectrum of targets that have been shown to be drivers of tumor growth” said Dr. Charles Baum, President and Chief Executive Officer of MethylGene Inc. “This molecule is a valuable addition to MethylGene’s oncology portfolio that is complementary to our MGCD265 program and has the potential to address unmet needs in patients with cancer” . About MG516 MG516 is a multi-targeted kinase inhibitor that covers a novel spectrum of targets including members of the Eph receptor family, the Met receptor, the Ret receptor tyrosine kinase, and all three vascular endothelial growth factor receptors (VEGFR 1, 2, 3). Eph is over-expressed in several cancers including gastric, breast, prostate and esophageal and is associated with resistance to HER2 inhibitors. Ret is expressed and has a role in medullary thyroid carcinoma, and recent data suggest a possible role as a driver of growth in lung cancer. MG516 has demonstrated potent inhibition of kinases in vitro, in multiple cell-based assays and has shown up to 100% of tumor growth inhibition in vivo against a number of tumor types in xenograft studies. In preclinical models anti-tumor activity is achieved at low doses and MG516 is well tolerated without significant weight loss or myelosuppression. MG516 is in advanced preclinical development and ready to commence IND-enabling studies. About MethylGene MethylGene Inc. (TSX:MYG) is a drug development company that is advancing novel therapeutics for the treatment of patients with cancer and infectious disease in human clinical trials. The Company’s lead clinical stage product candidates are: MGCD265, a multi-targeted receptor tyrosine kinase inhibitor that is in Phase I/II clinical trials for patients with solid tumors and MGCD290, an oral antifungal agent targeting the fungal Hos2 enzyme that was in Phase II trials for vulvovaginal candidiasis. MethylGene owns all rights to its lead product candidates, and has partnerships with Otsuka Pharmaceutical Co. Ltd., Taiho Pharmaceutical Co. Ltd., and EnVivo Pharmaceuticals, Inc. for its other pipeline programs. Investor Relations Contact: MethylGene, Inc. Mark J. Gergen Executive Vice President & COO Phone: 858-546-2902 Tracey Rowlands, Ph.D. Manager Business and Corporate Development Phone: 514-337-3333 ext. 512 ir@methylgene.com Thomas Hoffmann Vice President The Trout Group LLC Phone: 646-378-2931 thoffmann@troutgroup.com Certain statements contained in this news release, other than statements of fact that are independently verifiable at the date hereof, may constitute forward-looking information and forward-looking statements (collectively “forward-looking statements” within the meaning of applicable securities laws). Such statements, based as they are on the current expectations of management of MethylGene and upon what management believes to be reasonable assumptions, inherently involve numerous risks and uncertainties, known and unknown, many of which are beyond MethylGene’s control. Such statements can usually be identified by the use of words such as “may”, “would”, “believe”, “plan”, “estimate” and other similar terminology, or state that certain actions, events or results “may” or “would” be taken, occur or be achieved These risks and uncertainties could cause future results, performance or achievements to differ significantly from the results, performance or achievements expressed or implied by such forward-looking statements. Such results, performance or achievements include, but are not limited to, the timing and effects of regulatory action; the continuation of collaborations; the results of clinical trials; the timing of enrollment or completion of clinical trials; the success, efficacy or safety of MGCD265, MGCD290 or our other programs; the ability to scale up, formulate and manufacture sufficient GMP, clinical or commercialization quantities of MGCD265, MGCD290 or our other products, and the relative success or the lack of success in developing and gaining regulatory approval and/or market acceptance for any compound or new product including MGCD265 or MGCD290. Such risks include, but are not limited to, the impact of general economic conditions, economic conditions in the pharmaceutical industry, changes in the regulatory environment in the jurisdictions in which MethylGene does business, stock market volatility, fluctuations in costs, expectations with respect to our intellectual property position and our ability to protect our intellectual property and operate our business without infringing upon the intellectual property rights of others, changes in the competitive landscape including changes in the standard of care for the various indications in which MethylGene is involved, and changes to the competitive environment due to consolidation, as well as other risks, as described in MethylGene’s Annual Information Form under the heading ”Risk Factors” which you are urged to read, and all other documents filed by the Company that can be found at Consequently, actual future results may differ materially from the anticipated results expressed in the forward-looking statements. The reader should not place undue reliance on the forward-looking statements included in this news release. These statements speak only as of the date they are made and MethylGene expressly disclaims any duty, obligation or undertaking to release publicly any updates or revisions to any forward-looking statements contained herein to reflect any change in MethylGene’s expectations with regard thereto of any change in events, conditions or circumstances on which any such statements are based except in accordance with law

CollaborateAACR

29 May 2012

·www.biospace.com

MethylGene to Present MGCD265 Data at the 2012 American Society of Clinical Oncology Annual Meeting

Montreal, Canada. May 29, 2012 – MethylGene Inc. (TSX:MYG) today announced that clinical data for its Met/VEGF-R kinase inhibitor, MGCD265, will be presented at the 2012 ASCO Annual Meeting to be held in Chicago, Illinois from June 1 to 5, 2012. This poster presentation will highlight the safety pro MGCD265 when used as a monotherapy in this ongoing dose-escalation study. Poster Presentation MGCD265, a multitargeted oral tyrosine kinase receptor inhibitor of Met and VEGFR: Dose-escalation Phase I study. Date and Time: Monday June 4, 8:00 AM to 12:00 PM (CT) Session: Developmental Therapeutics - Experimental Therapeutics Abstract No.: 3039 Location: S Hall A2 About MGCD265 MGCD265 is a novel, oral small molecule inhibitor that targets a unique spectrum of receptor tyrosine kinases: Met, VEGFR 1, 2, and 3, Tie-2 and Ron. These kinases play key roles in tumor development, survival and metastasis as well as the inappropriate formation of blood vessels (angiogenesis) that nourish the tumor. MGCD265 has completed one Phase 1 single agent study, and is nearing completion of one Phase 1 single agent clinical trial and one Phase 1/2 combination clinical trial (with erlotinib and docetaxel) in solid tumors. About MethylGene MethylGene Inc. (TSX:MYG) is a small molecule drug development company that is advancing two novel therapeutics for cancer and infectious disease in human clinical trials. The Company’s lead product candidates are: MGCD290, an oral antifungal agent targeting the fungal Hos2 enzyme that is currently in Phase 2 trials for vulvovaginal candidiasis, and MGCD265, an oral Met/VEGF receptor kinase inhibitor that is in Phase 1/2 clinical trials for solid tumor cancers. MethylGene owns all rights to its lead product candidates, and has partnerships with Otsuka Pharmaceutical Co. Ltd., Taiho Pharmaceutical Co. Ltd., and EnVivo Pharmaceuticals, Inc. for its other pipeline programs. Investor Relations Contact: Joseph Walewicz, CFA Vice President, Business & Corporate Development MethylGene Inc. Phone: 514-337-3333 ext. 373 ir@methylgene.com Thomas Fechtner Vice President The Trout Group LLC Phone: 646-378-2931 tfechtner@troutgroup.com

CollaborateSmall molecular drugASCO

100 Deals associated with Glesatinib

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D11136	-	-	DB06302

R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
metastatic non-small cell lung cancer	Phase 2	US	Mirati Therapeutics, Inc.	01 Oct 2015
metastatic non-small cell lung cancer	Phase 2	AU	Mirati Therapeutics, Inc.	01 Oct 2015
metastatic non-small cell lung cancer	Phase 2	CA	Mirati Therapeutics, Inc.	01 Oct 2015
metastatic non-small cell lung cancer	Phase 2	HU	Mirati Therapeutics, Inc.	01 Oct 2015
metastatic non-small cell lung cancer	Phase 2	IT	Mirati Therapeutics, Inc.	01 Oct 2015
metastatic non-small cell lung cancer	Phase 2	PL	Mirati Therapeutics, Inc.	01 Oct 2015
metastatic non-small cell lung cancer	Phase 2	KR	Mirati Therapeutics, Inc.	01 Oct 2015
metastatic non-small cell lung cancer	Phase 2	TW	Mirati Therapeutics, Inc.	01 Oct 2015
metastatic non-small cell lung cancer	Phase 2	GB	Mirati Therapeutics, Inc.	01 Oct 2015
Non-Small Cell Lung Cancer	Phase 2	CN	Mirati Therapeutics, Inc.	01 Oct 2015

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT02954991 (CTgov)	Phase 2	metastatic non-small cell lung cancer	161	Glesatinib+nivolumab	dfznxqpxgy(sjmoseoefy) = zutxqlgqoe pewnjmjbuo (bpyuguejwh, ricdgvnvbe - tlxnptjfij) View more	-	22 Apr 2024
NCT00697632 (Pubmed)	Phase 1	Advanced Malignant Solid Neoplasm \| Non-Small Cell Lung Cancer	180	Glesatinib	gcknhqsbif(ydkmafvoei) = sfwrfydnei rxqudhsjni (emtwtljwch ) View more	-	02 Dec 2022
NCT00697632 (ASCO2016)	Phase 1	HR-positive/HER2-low Solid Tumors	18	MGCD265 softgel capsules	wqldntdvgk(ojfyrzeolt) = ntucgibong gaorogehof (tnrsuojyrg ) View more	-	20 May 2016
NCT00697632 (ASCO2016)	Phase 1	HR-positive/HER2-low Solid Tumors	18	MGCD265 SDD tablets	wqldntdvgk(ojfyrzeolt) = inmbsuromd gaorogehof (tnrsuojyrg ) View more	-	20 May 2016
NCT00697632 (ASCO2015) Manual	Phase 1	HR-positive/HER2-low Solid Tumors	12	Glesatinib	eegdiiaufu(epfswizatj) = At 1200 mg BID, 2 out of 6 evaluable pts experienced DLT (G3 fatigue; G3 diarrhea). lohzzyyihf (xpsveroodu ) View more	Positive	20 May 2015
ASCO2012	Phase 1	HR-positive/HER2-low Solid Tumors	45	MGCD265	vxwmgyqxof(zgnhreqcsb) = One out of 3 pts with NSCLC, who was positive for activating EGFR mutation, experienced a partial response (duration of response of 8 cycles) kplpwbhnkd (bvevpdjrjv )	-	20 May 2012
ASCO2012	Phase 1	HR-positive/HER2-low Solid Tumors	34	MGCD265	johihycenm(gxjmvumfwn) = llelgvhkpr qffwacrjya (fqdbqneisq )	-	20 May 2012
study 265-102 (ASCO2010)	Phase 1	Advanced cancer	28	MGCD265	xvwxfgybqs(huptxmppbz) = diarrhea, nausea, neutropenia, and intermittent dizziness vhutjvwnhd (sgafktrssy ) View more	-	20 May 2010

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