UPDATE — ArQule Presents Data on Tivantinib and Proprietary Pipeline at AACR-NCI-EORTC Conference

On November 09, 2015 ArQule, Inc. (Nasdaq:ARQL) reported the results of preclinical and clinical studies focusing on tivantinib, ARQ 087, ARQ 092, and ARQ 751 (Press release, ArQule, NOV 9, 2015, View Source [SID:1234508132]). The data were presented at the AACR (Free AACR Whitepaper)-NCI-EORTC meeting on November 7th, 2015. The poster presentations can be accessed in the "Investor and Media" section of our website, www.arqule.com, under "Recent Data Presentations."

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For the first time, data from an exploratory sub-analysis of the MARQUEE trial with tivantinib in non-small cell lung cancer in patients with advanced disease and epidermal growth factor receptor (EGFR) mutations were presented. The data showed tivantinib, when added to erlotinib, increased progression-free survival to 13 months compared to 7.5 months in the erlotinib plus placebo arm. The sub-analysis included 109 patients of which 56 were in the combination tivantinib plus erlotinib arm of the trial. The data were highlighted in an AACR (Free AACR Whitepaper) press release and press conference.

"The data from the sub-analysis of the MARQUEE trial supports our focus on precision medicine," said Brian Schwartz, M.D., Head of Research and Development and Chief Medical Officer at ArQule. "Although the study did not meet its primary endpoint, this analysis is encouraging and offers evidence that tivantinib when dosed in a specific patient population can provide substantial benefit."

Additionally, the company presented pre-clinical and clinical data on its early stage proprietary pipeline that support ArQule’s efforts to address the needs of patients in therapeutic areas of high unmet need through precision medicine. Data presented on FGFR inhibitor, ARQ 087, demonstrate that FGFR2 dysregulation correlates with efficacy and supports the on-going phase 2 trial in intrahepatic cholangiocarcinoma. Similarly, data presented on AKT inhibitors, ARQ 092 and ARQ 751, demonstrate that both drugs inhibit AKT and provide strong rationale for further studies in patients harboring AKT1 and PI3K mutations.

"Data presented at this year’s AACR (Free AACR Whitepaper)-NCI-EORTC conference are part of ArQule’s translational effort to connect preclinical and clinical research and guide a true precision medicine endeavor," said Giovanni Abbadessa, Vice President of Clinical Development, Translational Medicine and Medical Affairs at ArQule. "Both ARQ 092 and ARQ 087 have shown single-agent activity in vitro, in vivo and in patients in cancers driven by genetic alterations of their respective targets, AKT and FGFR. In addition, these pre-clinical data find confirmation in the clinical results achieved by ARQ 087 and ARQ 092 in their respective phase 1 clinical trials in genetically-altered endometrial and breast cancer and in FGFR2-driven cholangiocarcinoma, respectively. Combinability data reported for both experimental drugs with standard therapies may allow even more development options for the future."

Precision Medicine

Tivantinib is enrolling in two biomarker-driven phase 3 trials, METIV-HCC and JET-HCC. ARQ 087 is enrolling in a biomarker-driven phase 2 trial in intrahepatic cholangiocarcinoma (iCCA) with FGFR translocations. ARQ 092 is enrolling in a phase 1b biomarker-driven trial in patients with AKT and PI3K activating mutations including patients with breast, endometrial and ovarian cancers.

About MET and tivantinib (ARQ 197)

Tivantinib is an orally administered, selective inhibitor of MET, a receptor tyrosine kinase, which is currently in Phase 3 clinical trials. In healthy adult cells, MET can be present in normal levels to support natural cellular function, but in cancer cells, MET can be inappropriately and continuously activated. When abnormally activated, MET plays multiple roles in aspects of human cancer, including cancer cell growth, survival, angiogenesis, invasion and metastasis. The activation of certain cell signaling pathways, including MET, has also been associated with the development of resistance to anti-EGFR (epidermal growth factor receptor) antibodies such as cetuximab and panitumumab.

Pre-clinical data have demonstrated that tivantinib inhibits MET activation in a range of human tumor cell lines and shows anti-tumor activity against several human tumor xenografts. In clinical trials to date, treatment with tivantinib has been generally well tolerated and has shown clinical activity in a number of tumors. Tivantinib has not yet been approved for any indication in any country.

In December 2008, ArQule and Daiichi Sankyo signed a license, co-development and co-commercialization agreement for tivantinib in the U.S., Europe, South America and the rest of the world, excluding Japan, China (including Hong Kong), South Korea and Taiwan.

About the AKT Pathway, ARQ 092 and ARQ 751

ARQ 092 and ARQ 751 are orally available, selective small molecule inhibitors of the AKT kinase. The AKT pathway when abnormally activated is implicated in multiple oncogenic processes such as cell proliferation and apoptosis. This pathway has emerged as a target of potential therapeutic relevance for compounds that inhibit its activity, which has been linked to a variety of cancers as well as to select non-oncology indications.

ARQ 092, the lead compound in ArQule’s AKT program, has completed Phase 1a clinical testing and has advanced into Phase 1b expansion testing in cohorts of patients with endometrial cancer, lymphoma and tumors harboring either AKT or PI3K mutations. A number of next-generation compounds in the Company’s AKT program are in early to late stages of pre-clinical development. The company plans to file an Investigational New Drug (IND) application by the end of 2015 for ARQ 751, a next generation AKT inhibitor.

About FGFR and ARQ 087

ARQ 087 is a multi-kinase inhibitor designed to preferentially inhibit the fibroblast growth factor receptor ("FGFR") family with demonstrated efficacy in FGFR2 amplified tumors. The FGFR pathway is disrupted in several ways in human cancer, thus providing numerous therapeutic targets for an inhibitor of this pathway. ARQ 087 has demonstrated inhibition of tumor growth and downstream signaling in vivo in tumors whose growth is driven by these targets.

Signals of single agent activity with this compound were observed in Phase 1a testing. Phase 1b expansion cohorts with ARQ 087 include patients with cholangiocarcinoma and adrenocortical tumors, as well as those with FGFR translocations, amplification and mutations. Clinical development of ARQ 087 has advanced into Phase 2 for intrahepatic cholangiocarcinoma ("iCCA") following the observation of two confirmed partial responses in this patient population in the Phase 1 portion of the program.

10-Q – Quarterly report [Sections 13 or 15(d)]

(Filing, 10-Q, CellCeutix, NOV 9, 2015, View Source [SID:1234508150])

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10-Q – Quarterly report [Sections 13 or 15(d)]

(Filing, 10-Q, PTC Therapeutics, NOV 9, 2015, View Source [SID:1234508175])

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Foundation Medicine and Collaborators to Present New Clinical Data Supporting Comprehensive Genomic Profiling in Advanced Sarcomas and Hematologic Malignancies with FoundationOne® Heme

On November 9, 2015 Foundation Medicine, Inc. (NASDAQ:FMI) reported that the company and its collaborators will present three oral and four poster presentations at the 2015 American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting taking place December 5 – 8, 2015 in Orlando, Florida (Press release, Foundation Medicine, NOV 9, 2015, View Source [SID:1234508109]). Collectively, the presentations will focus on the application of FoundationOne Heme to identify druggable genomic alterations, inform personalized treatment strategies and improve clinical outcomes across a broad range of sarcomas and hematologic malignancies.

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FoundationOne Heme is a comprehensive genomic profile that analyzes DNA in 405 genes and RNA in 265 genes that are most commonly altered in hematologic malignancies and sarcomas. The assay provides oncologists and pathologists with clinically relevant genomic alterations to guide treatment options for patients based on the genomic profile of their cancer.

The schedule for oral presentations by Foundation Medicine and/or its collaborators is as follows:

Session Date & Time: Saturday, December 5, 2015, from 12:00-1:30 p.m. ET
Presentation Time: 12:45 p.m. ET
Title: Genomic and Proteomic Analysis of Primary Chemoresistance and Induction Failure in Acute Myeloid Leukemia
Publication Number: 88
Location: Tangerine 3 (WF3-4), Level 2
Session: 617 – Acute Myeloid Leukemia: Biology, Cytogenetics and Molecular Markers in Diagnosis and Prognosis: Omics-based Approaches for the Identification of Novel Genetic Modalities in AML
Presenter: Fiona Brown, Ph.D., research fellow, Memorial Sloan-Kettering Cancer Center
Collaborators: Memorial Sloan-Kettering Cancer Center, Dana-Farber Cancer Institute, Children’s Hospital Boston, Children’s Oncology Group, Fred Hutchinson Cancer Research Center, The University of Texas MD Anderson Cancer Center, The Ohio State University Comprehensive Cancer Center, Harvard Medical School

Session Date & Time: Sunday, December 6, 2015, from 4:30-6:00 p.m. ET
Presentation Time: 5:45 p.m. ET
Title: Comprehensive Genomic Profiling of Multiple Myeloma in the Course of Clinical Care Identifies Targetable and Prognostically Significant Genomic Alterations
Publication Number: 369
Location: W224ABEF
Session: 651 – Myeloma: Biology and Pathophysiology, Excluding Therapy: Novel Technologies to Evaluate Biology and Prognosis
Presenter: Christopher Heuck, M.D., assistant professor of medicine, Myeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences
Collaborators: Myeloma Institute for Research and Therapy

Session Date & Time: Monday, December 7, 2015 from 7:00-8:30 a.m. ET
Presentation Time: 7:00 a.m. ET
Title: Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms
Publication Number: 481
Location: W331
Session: 635 – Myeloproliferative Syndromes: Basic Science I
Presenter: Benjamin Durham, M.D., research fellow, Memorial Sloan-Kettering Cancer Center
Collaborators: Memorial Sloan-Kettering Cancer Center

The schedule for poster presentations by Foundation Medicine and/or its collaborators is as follows:

Poster Display: Saturday, December 5, 2015 from 9:00 a.m.-7:30 p.m. ET
Poster Presentation: Saturday, December 5, 2015 from 5:30-7:30 p.m. ET
Title: Integrated DNA/RNA Profiling for Somatic Alterations in Adult B-cell ALL
Publication Number: 1422
Poster Display Location: Hall A2-A3
Poster Presentation Location: Hall A2-A3
Session: 618 – Acute Lymphoblastic Leukemia: Biology, Cytogenetics and Molecular Markers in Diagnosis and Prognosis: Poster I
Presenter: Franck Rapaport, Ph.D., computational research leader, Leukemia Center, Memorial Sloan-Kettering Cancer Center
Collaborators: Memorial Sloan-Kettering Cancer Center, Montefiore Medical Center, Mayo Clinic, University of Pennsylvania, Shaare Zedek Medical Center, Northwestern University Feinberg School of Medicine, Weill Cornell Medical College

Poster Display: Sunday, December 6, 2015 from 9:00 a.m.-8:00 p.m. ET
Poster Presentation: Sunday, December 6, 2015 from 6:00-8:00 p.m. ET
Title: Predictive and Prognostic Significance of Comprehensive Genomic Profiling in Patients with Diffuse Large B-cell Lymphoma
Publication Number: 2651
Poster Display Location: Hall A2-A3
Poster Presentation Location: Hall A2-A3
Session: 622 – Non-Hodgkin Lymphoma: Biology, Excluding Therapy: Poster II
Presenter: Jie He, senior manager, computational biology analysis, Foundation Medicine

Poster Display: Sunday, December 6, 2015 from 9:00 a.m.-8:00 p.m. ET
Poster Presentation: Sunday, December 6, 2015 from 6:00-8:00 p.m. ET
Title: Defining the Incidence and Clinical Impact of Genomic Alterations Across Different Histologic Types of Lymphoma Using a Clinically Validated Comprehensive Targeted Sequencing Assay
Publication Number: 2668
Poster Display Location: Hall A2-A3
Poster Presentation Location: Hall A2-A3
Session: 622 – Non-Hodgkin Lymphoma: Biology, Excluding Therapy: Poster III
Presenter: Connie Lee Batlevi, M.D., Ph.D., hematology/oncology fellow, Memorial Sloan-Kettering Cancer Center
Collaborators: Memorial Sloan-Kettering Cancer Center

Poster Display: Monday, December 7, 2015 from 10:00 a.m.-8:00 p.m. ET
Poster Presentation: Monday, December 7, 2015 from 6:00-8:00 p.m. ET
Title: Comprehensive Genomic Profiling (CGP) of Angioimmunoblastic T-cell Lymphoma (AITL) to Prospectively Inform Diagnosis and Clinical Management
Publication Number: 3898
Poster Display Location: Hall A2-A3
Poster Presentation Location: Hall A2-A3
Session: 622 – Non-Hodgkin Lymphoma: Biology, Excluding Therapy: Poster III
Presenter: Tariq Mughal, M.D., vice president, medical affairs, Foundation Medicine
Collaborators: Memorial Sloan-Kettering Cancer Center, Tufts University Medical Center

8-K – Current report

On November 9, 2015 Galectin Therapeutics Inc. (NASDAQ: GALT), the leading developer of therapeutics that target galectin proteins to treat fibrosis and cancer, reported financial results for the three and nine months ended September 30, 2015 and provided a business update (Filing, 8-K, Galectin Therapeutics, NOV 9, 2015, View Source [SID:1234508135]). These results are included in the Company’s Quarterly Report on Form 10-Q, which has been filed with the U.S. Securities and Exchange Commission.

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Management commentary

"Galectin Therapeutics has never been in a better position advancing the development of our galectin-3 inhibitor in non-alcoholic steatohepatitis (NASH) and other therapeutic indications," said Jim C. Czirr, executive chairman of the company. "Our pipeline has progressed considerably during the third quarter and recent weeks, and we now have five clinical studies underway with our proprietary compound, GR-MD-02, in four different indications.

"We began a second Phase 2 study in NASH with advanced fibrosis, the NASH-FX study, during the quarter, and we continued to enroll patients in our Phase 2 study in NASH with cirrhosis, the NASH-CX study. We also began a pilot study to evaluate the potential efficacy of GR-MD-02 in patients with moderate-to-severe plaque psoriasis. More recently, after the close of the quarter we announced that the Providence Portland Medical Center submitted an Investigational New Drug (IND) application to study GR-MD-02 in combination with Keytruda in metastatic melanoma. This is in addition to its ongoing study of GR-MD-02 in combination with Yervoy in the same indication. To support this increased activity at Galectin, during the quarter we hired an industry veteran, Adam E. Allgood, Pharm.D., R.Ph. as executive director of clinical development," Mr. Czirr added.

Peter G. Traber, M.D., president, chief executive officer and chief medical officer, said, "NASH has been a topic of keen interest within the medical community as this disease appears to be overtaking hepatitis C as the number one cause of liver transplants, affecting up to 6 million people in the U.S. We are very excited about the potential of GR-MD-02 to treat the fibrosis and cirrhosis that can accompany NASH, and we are working hard to make efficacious treatment a reality.

"We are very pleased with the pace of our clinical studies and remain on track with our stated timelines," added Dr. Traber. "The NASH-CX trial, which if successful has potential to be a component of a pivotal study, began enrolling patients with NASH cirrhosis, with 156 patients in total to be enrolled. Patients are being evaluated with either 8 mg/kg of GR-MD-02, 2 mg/kg of GR-MD-02 or placebo, and are being randomized 1:1:1. The primary endpoint for this trial is change in hepatic venous pressure gradient (HVPG) compared with placebo, with secondary endpoints of fibrosis stage on biopsy as well as the percent of collagen on biopsy at one year of treatment. Additionally, the HVPG and liver biopsy measurements will be correlated with non-invasive measurements of liver fibrosis and function using FibroScan and 13C-methacetin breath test, respectively. We expect top-line data readout by the end of 2017.

Dr. Traber continued, "The NASH-FX trial in 30 patients with NASH with advanced fibrosis, but not cirrhosis, is proceeding as planned. This four-month treatment trial will evaluate the efficacy of 8 mg/kg of GR-MD-02 versus placebo, using non-invasive endpoints. LiverMultiScan, a multi-parametric nuclear magnetic resonance imaging method developed by Perspectum Diagnostics, will be used to measure the change in inflammation and fibrosis as a primary endpoint. The secondary goal is to compare the primary endpoint of LiverMultiScan with two secondary endpoints that are non-invasive measures of liver stiffness that correlate with fibrosis, magnetic resonance elastography and FibroScan. We expect data readout from the NASH-FX trial in the third quarter of 2016.

"We have also begun screening patients with moderate-to-severe plaque psoriasis in a proof-of-concept, open-label Phase 2a trial. In this trial 10 patients will be treated with 8mg/kg of GR-MD-02 every 2 weeks over 90 days. Research has shown that galectin-3 is increased in the skin of psoriasis patients, thus we have good support for the mechanism of action of our compound. In addition, as previously disclosed, one subject in our Phase 1 NASH study had an apparent remission of psoriasis. As such, we believe it is worthwhile to explore this indication further in this small study.

"We expect that the Portland Cancer Center will begin enrolling patients in its Phase 1b study of GR-MD-02 in combination with Keytruda within the coming weeks, following the filing of its IND in October. Keytruda is an immune checkpoint inhibitor indicated for patients whose melanoma had progressed after treatment with Yervoy or targeted therapy in melanomas that have a BRAF mutation. Preclinical data show that GR-MD-02 holds potential to increase the effectiveness of other therapies and represents a promising approach to enhance cancer immunotherapy. GR-MD-02 is also the subject of an ongoing study in combination with Yervoy being conducted by same investigators at the Portland Cancer Center. We are very pleased to be supplying our compound to the investigators," Dr. Traber concluded.

Additional information about the Company’s clinical development program and clinical trials is available on the CEO Perspectives website at View Source

Financial Results
For the three months ended September 30, 2015, the Company reported a net loss applicable to common stockholders of $6.2 million, or ($0.26) per share, compared with a net loss applicable to common stockholders of $3.9 million, or ($0.17) per share, for three months ended September 30, 2014. The increase in net loss applicable to common stockholders is largely due to higher research and development expenses related to the Company’s Phase 2 clinical program.
Research and development expense for the three months ended September 30, 2015 was $4.5 million, compared with $2.0 million for three months ended September 30, 2014. The increase is primarily due to increased costs related to the Company’s Phase 2 clinical program.

General and administrative expense for the three months ended September 30, 2015 was $1.4 million, compared with $1.5 million for the three months ended September 30, 2014. The primary reason for the decrease was related to a decrease in stock-based compensation expense in the three months ended September 30, 2015, compared with 2014.

For the nine months ended September 30, 2015, the Company reported a net loss applicable to common stockholders of $16.2 million, or ($0.69) per share, compared with a net loss applicable to common stockholders of $13.0 million, or ($0.60) per share, for the nine months ended September 30, 2014. The increase in net loss applicable to common stockholders is largely due to higher research and development expenses related to the Company’s Phase 2 clinical program.

Research and development expense for the nine months ended September 30, 2015 was $10.2 million, compared with $6.3 million in the prior year’s period. The higher research and development expense is related to increased expenses associated with the Company’s Phase 2 clinical studies.

General and administrative expense for the nine months ended September 30, 2015 was $5.2 million, compared with $5.4 million for the nine months ended September 30, 2014. The decline was due to lower stock-based compensation expense.
As of September 30, 2015, the Company had $21.3 million of non-restricted cash and cash equivalents available to fund future operations. The Company believes that its cash on hand as of September 30, 2015 is sufficient to fund currently planned operations and research and development activities through September 30, 2016.