On December 7, 2016 Cascadian Therapeutics, Inc. (NASDAQ:CASC), a clinical-stage biopharmaceutical company, reported that following a recent meeting with the U.S. Food and Drug Administration (FDA) and discussions with the Company’s external Steering Committee, it has amended the HER2CLIMB Phase 2 clinical trial of tucatinib (also known as ONT-380) by increasing the sample size so that, if successful, the trial could serve as a single pivotal study to support registration (Press release, Cascadian Therapeutics, DEC 7, 2016, View Source [SID1234516981]). This decision is supported by the most recent data from the Company’s ongoing Phase 1b study evaluating the same "triplet combination" therapy being investigated in the amended Phase 2 trial, which is tucatinib in combination with capecitabine and trastuzumab for patients with metastatic or locally advanced HER2-positive breast cancer, including patients with and without brain metastases. Tucatinib is an oral, small molecule kinase inhibitor that is highly selective for HER2 without significant inhibition of EGFR. Schedule your 30 min Free 1stOncology Demo! HER2CLIMB is an ongoing randomized, controlled pivotal trial evaluating tucatinib in combination with trastuzumab (Herceptin) and capecitabine (Xeloda) in heavily pre-treated patients with advanced HER2-positive breast cancer with or without brain metastases.
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"We are extremely pleased with the outcome of our recent interactions with the FDA, and we have decided to amend the current Phase 2 clinical trial of tucatinib so that, if successful, HER2CLIMB could serve as a single pivotal registration trial and potentially provide us with a more efficient path to market," commented Scott Myers, President and CEO of Cascadian Therapeutics. "We look forward to continuing a collaborative relationship with the agency and our clinical investigators as we advance the development of tucatinib in combination in the third-line metastatic breast cancer setting where there is no single standard-of-care and a need for more tolerable therapeutic options. The improvement in the updated data from our Phase 1b "triplet combination" study reinforces our strategy with tucatinib in this patient population."
Updated Phase 1b trial results for the triplet combination show that the combination (tucatinib with capecitabine and trastuzumab) continues to be well tolerated, with the updated median progression-free survival (PFS) increasing to 7.8 months, an overall response rate (ORR) of 61 percent and a median duration of response (MDR) of 10 months. Patients in the Phase 1b triplet combination previously received a median of 3 HER2-targeted agents, such as trastuzumab, pertuzumab, lapatinib or T-DM1. Poster presentations on the amended HER2CLIMB pivotal trial and the updated Phase 1b "triplet combination" trial data will be presented at the 2016 San Antonio Breast Cancer Symposium (SABCS), December 6-10, 2016.
"The more mature dataset from the Phase 1b trial continues to show tucatinib may be combined with other current targeted therapies to achieve durable responses in patients who have received multiple prior lines of therapy," said Erika Hamilton, M.D., Director of Breast and Gynecology Cancer Research at Sarah Cannon Research Institute. "Tucatinib in combination appears to be well-tolerated, potentially making it a highly desirable HER2 therapy for a patient population that vitally needs new options. An active agent showing systemic activity, with a tolerable safety profile and early signs of activity in HER2-positive brain metastases, would represent a meaningful advancement in treating metastatic breast cancer."
HER2CLIMB Pivotal Trial
HER2CLIMB is a randomized (2:1), double-blind, controlled pivotal clinical trial comparing tucatinib vs. placebo in combination with capecitabine and trastuzumab in patients with locally advanced or metastatic HER2-positive breast cancer who have had prior treatment with a taxane, trastuzumab, pertuzumab and T-DM1. Following a meeting with the FDA, the primary endpoint remains PFS based upon independent radiologic review, and the sample size will increase to approximately 480 patients, including patients already enrolled in the trial. Key objectives related to assessing activity in brain metastases include a key secondary endpoint of PFS in a subset of patients with brain metastases. All patients will be followed for overall survival. HER2CLIMB is currently enrolling in the United States and Canada and is expected to expand into Europe, Australia and Israel. Details of the amended HER2CLIMB clinical trial design will be presented in a poster session (OT1-02-09) at SABCS on Wednesday, December 7, 2016 beginning at 5:00 p.m. CST.
Updated Phase 1b Triplet Study Findings at SABCS
Results reported in June 2016 showed a median PFS of 6.3 months and ORR of 58 percent. Updated data from the SABCS poster (P4-21-01) of the Phase 1b study show encouraging safety and anti-tumor activity in patients with and without brain metastases, with an updated median PFS of 7.8 months (a 24 percent improvement over prior median PFS), ORR of 61 percent and a median duration of response of 10 months. Patients with and without brain metastases had similar response rate. The combination of tucatinib with trastuzumab and capecitabine was well-tolerated. Most treatment-emergent adverse events were Grade 1, with few tucatinib dose reductions and no required prophylactic use of antidiarrheal agents. Updated results will be presented in a poster session at SABCS on Friday, December 9, 2016 beginning at 7:30 a.m. CST.
About Tucatinib
Tucatinib is an orally bioavailable, potent tyrosine kinase inhibitor that is highly selective for HER2 without significant inhibition of EGFR. Inhibition of EGFR has been associated with significant toxicities, including skin rash and diarrhea. Tucatinib has shown activity as a single agent and in combination with both chemotherapy and other HER2 directed agents such as trastuzumab.1 Studies of tucatinib in these combinations have shown activity both systemically and in brain metastases. HER2 is a growth factor receptor that is overexpressed in multiple cancers, including breast, ovarian and gastric cancers. HER2 mediates cell growth, differentiation and survival. Tumors that overexpress HER2 are more aggressive and historically have been associated with poor overall survival, compared with HER2-negative cancers.
About HER2-Positive Metastatic Breast Cancer
Patients with HER2-positive breast cancer have tumors with high levels of a protein called human epidermal growth factor receptor 2 (HER2), which promotes the aggressive spread of cancer cells. The American Cancer Society estimates that 20-25 percent of the approximately 234,000 annual breast cancer diagnoses in the U.S. are HER2-positive. Historically, HER2 disease has been associated with shorter survival times as well as a higher risk of recurrence and CNS disease (brain metastases). Approximately 30 to 50 percent of HER2-positive breast cancer patients develop brain metastases over time.2,3 Over the past two decades, the approvals of four targeted treatments (trastuzumab, pertuzumab, lapatinib, and ado-trastuzumab emtansine) have led to improved time to progression and survival rates of HER2-positive patients. Despite these advances, there is still a significant need for new therapies that can impact metastatic disease, including brain metastases, and be tolerated for longer periods of time.
Author: [email protected]
Arvinas Collaborators Present Data on BET PROTAC Degraders at 2016 ASH Annual Meeting
On December 6, 2016 Arvinas LLC, a private biotechnology company creating a new class of drugs known as PROTACs which function via targeted protein degradation reported that preclinical data were presented by three Arvinas collaborators at the 2016 American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting in San Diego, CA (Press release, Arvinas, DEC 6, 2016, View Source [SID1234517044]). The data presented demonstrate superior efficacy of PROTACs targeting the BET (bromodomain and extraterminal domain) protein family when compared to BET inhibitors in preclinical models of lymphoma and leukemia.
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"The data further support our ongoing understanding of how the Arvinas BET PROTACs show pronounced efficacy improvements compared to BET inhibitors in in vitro and in vivo model systems. The advantages of BET degradation have now been demonstrated preclinically in a number of solid tumor and hematologic cancers including diffuse large B cell lymphoma, prostate cancer, ovarian cancer, mantle cell lymphoma and acute myeloid leukemia (AML)," said Manuel Litchman, M.D., President and CEO of Arvinas.
"These findings underscore the superior activity of BET PROTACs versus BET inhibitors against mantle cell lymphoma cells that are either sensitive or resistant to the drug ibrutinib, as well as against models of AML," said Kapil Bhalla, M.D., Professor of Leukemia at the University of Texas MD Anderson Cancer Center.
In a podium presentation titled "Novel BET PROTACs Exert Potent Single Agent and Synergistic Activity with Ibrutinib and Venetoclax Against Human Mantle Cell Lymphoma Cells" and presented by Dr. Bhalla, data show:
Compared to BET inhibitors, in primary mantle cell lymphoma (MCL) cells and MCL cell lines, BET PROTACs provide greater down-regulation of the expression of genes important to tumor growth and survival, greater killing of cells resistant to ibrutinib and greater inhibition of the growth of ibrutinib-resistant MCL xenografts alone and in combination with rationally selected targeted agents.
Dr. Sujan Piya of the University of Texas MD Anderson Cancer Center presented data on Arvinas BET PROTAC ARV-825 in a podium presentation titled "BRD4 PROTAC ARV-825 Causes Sustained Degradation of BRD4 and Modulation of Chemokine Receptors, Cell Adhesion and Metabolic Targets in Leukemia Resulting in Profound Anti-Leukemic Effects."
As a single agent, ARV-825 demonstrated substantial activity across multiple models of AML, including cell lines, primary AML blasts and a mouse model of human leukemia.
In all tested cell lines and primary cells, the BET PROTAC was significantly more potent than a BET inhibitor.
Importantly, in a co-culture model, ARV-825 was shown to modulate the tumor microenvironment and metabolism to overcome stroma-mediated drug resistance.
Dr. Warren Fiskus of the University of Texas MD Anderson Cancer Center delivered a podium presentation titled "Superior Lethal Activity of Novel BET PROTAC Versus BET Inhibitor Against Post-Myeloproliferative Neoplasm Secondary AML Cells (sAML)."
Arvinas BET PROTACs were significantly more potent than a BET inhibitor in inducing apoptosis-driven cell death of patient-derived and cultured secondary AML (sAML) cells and caused greater depletion of several key sAML signaling and survival proteins.
Co-treatment of BET PROTAC ARV-825 and JAK inhibitor ruxolitinib showed synergistic lethality against sAML cells.
Notably, BET PROTACs both alone and in combination with either an HSP90 inhibitor or a BCL2/BcL-xL antagonist were highly active against JAK inhibitor-resistant sAML cells.
Compared to a BET inhibitor, treatment with BET-PROTAC ARV-771 significantly reduced leukemia growth and improved survival of mice engrafted with sAML cell xenografts.
Chi-Med Presents Pre-clinical Data for Selective Syk Inhibitor HMPL-523 at the 2016 American Society of Hematology Annual Meeting
On December 6, 2016 Hutchison China MediTech Limited ("Chi-Med") (AIM/Nasdaq: HCM) reported that data from a recent pre-clinical study, investigating the in vitro and in vivo anti-tumor activities of novel Spleen Tyrosine Kinase ("Syk") inhibitor, HMPL-523, was presented at the Annual Meeting of the American Society of Hematology (ASH) (Free ASH Whitepaper) ("ASH"), being held in San Diego, CA, USA from December 3 to December 6, 2016 (Press release, Hutchison China MediTech, DEC 6, 2016, http://www.chi-med.com/hmpl-523-data-at-ash-2016/ [SID1234516989]).
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Syk, a non-receptor type of tyrosine kinase, plays a pivotal role in the regulation of the B-cell receptor (BCR) signaling pathway, which regulates proliferation, differentiation and survival of B lymphocytes. The abnormal activation of BCR signaling is closely related to transformation and development of B-cell lymphoma.
Presentation Title: HMPL-523, a Novel Syk Inhibitor, Showed Anti-Tumor Activities in Vitro and in Vivo
Authors: Na Yang, Wei Deng, Qiaoling Sun, Junqing Liang, Linfang Wang, Shiming Fan, Renxiang Tang, Ying Yu, Junen Sun, Feng Zhou, Guangxiu Dai, Weiguo Qing, Weiguo Su and Yongxin Ren
Abstract No: 3970
Session: 605. Molecular Pharmacology, Drug Resistance—Lymphoid and Other Diseases
Date & Time: Monday, December 5, 2016, 6:00PM – 8:00PM (PST)
The presentation is available at www.chi-med.com/wp-content/uploads/2016/12/pre161206_523ash.pdf.
Potent anti-tumor activity and combination synergy with other therapies
In vitro in B-cell lymphoma cell lines with Syk/BCR dysregulation, HMPL-523 was found to block phosphorylation of B-cell linker protein as well as inhibit cell viability by inhibiting cell survival and increasing apoptotic rate. HMPL-523 also showed synergistic anti-tumor activity on human diffused large B-cell lymphoma cells, in combination with other drugs such as Phosphoinositide-3-Kinase δ inhibitors, B-cell lymphoma 2 family inhibitors, or chemotherapies. Potent anti-tumor activity was also demonstrated in nude mice bearing B-cell lymphoma xenograft tumors with Syk/BCR dysregulation.
Clinical development in oncology and immunology
In hematological malignancies, HMPL-523 is currently being studied in a Phase I dose escalation study, which was initiated in Australia in January 2016 and is expected to complete in the first half of 2017. This study is in patients with relapsed and/or refractory B-cell non-Hodgkin’s lymphoma or chronic lymphocytic leukemia for whom there is no standard therapy.
HMPL-523 is also being studied in immunological indications. Clinical data for HMPL-523 in a Phase I dose-escalating study in healthy volunteers in Australia was recently presented at the 2016 Annual Meeting of the American College of Rheumatology/Association of Rheumatology Health Professionals, which was held in November 2016. The detailed poster presentation can be viewed at www.chi-med.com/wp-content/uploads/2016/11/pre1611141.png. The Company plans to initiate a Phase II study in the U.S. in 2017.
About the ASH (Free ASH Whitepaper) Annual Meeting
The ASH (Free ASH Whitepaper) annual meeting, a scientific conference focused on malignant and non-malignant hematology, brings together more than 20,000 hematology professionals from around the world. The meeting provides an educational experience, with thousands of scientific abstracts highlighting the latest research in the field available for review, as well as the opportunity to network with a global community of professionals from every subspecialty.
About B-cell signaling
The BCR signaling pathway regulates proliferation, differentiation and survival of B lymphocytes, a major cellular component of the immune system. The abnormal activation of BCR signaling is closely related to transformation and development of hematological cancers (i.e. B-cell malignancies) including lymphoma and leukemia, as well as autoimmune diseases, such as rheumatoid arthritis. Targeted B-cell receptor signaling therapies, including monoclonal antibodies and small molecules, have been proven to be clinically effective for the treatment of B-cell malignancies, leading to scientific and commercial success.
Syk is a key protein involved in the B-cell signaling pathway.
Cellectar Biosciences Presents Poster at the 58th Annual Meeting of the American Society of Hematology
On December 6, 2016 Cellectar Biosciences, Inc. (Nasdaq: CLRB) (the "company"), an oncology-focused, clinical stage biotechnology company, reported that it presented a poster at the 58th Annual Meeting of the American Society of Hematology (ASH) (Free ASH Whitepaper) in San Diego, which provides highlights of the company’s ongoing Phase I dose escalation clinical study of CLR 131 to assess safety and tolerability of the compound in patients with relapsed or refractory multiple myeloma (Filing, 8-K, Cellectar Biosciences, DEC 6, 2016, View Source [SID1234516979]). The poster provided detailed data related to the first two study cohorts.
The poster followed patients from initial infusion of CLR 131, the company’s lead PDC radiotherapeutic, through November 1, 2016. Results demonstrated all eight evaluable patients (of the total of ten enrolled) achieving a minimum of stable disease. The poster also reported a mean of approximately three months of progression-free survival (PFS) in Cohort 1 and four months in Cohort 2. To date, one patient in Cohort 2 continues to experience PFS. Significantly, four of eight patients experienced a greater than 50 percent reduction in serum free light chains (FLC), which are a key efficacy indicator for multiple myeloma. Per the International Myeloma Working Group (IMWG) criteria, in the absence of M protein, an FLC reduction of 50 percent or greater, is defined as a partial response. Overall, Cohort 2 patients experienced a more significant FLC reduction and a more sustained FLC response versus Cohort 1, with the difference in reduction being maintained across the entire study, and increasing at the subsequent evaluation time points. Cohort 2 patients achieved a 20 percent greater reduction in FLC on day 22 than was experienced by patients in Cohort 1, a 38 percent greater reduction at Day 43 and 43 percent greater FLC reduction at the final evaluation time point, Day 64.
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Importantly, seven of eight evaluable patients achieved a reduction in either serum or urine M protein, which also are key efficacy indicators for multiple myeloma. Similar to the FLC marker, the Cohort 2 reduction of M protein was more sustained with the patients experiencing continued reduction in M protein beyond day 64. It is also important to note that based upon M protein reduction 38 percent of patients experienced a minimal response at these low, one-time doses.
The primary endpoint for this study is to determine the safety and tolerability of CLR 131 in a heavily pre-treated patient population. Evaluable study patients received an average of four prior lines of treatment. The adverse event profile in both cohorts was similar and showed no dose dependency. While the leading adverse events were leukopenia and thrombocytopenia (30 percent each) with a median grade of 2 (mild to moderate) for both, there have been no dose-limiting toxicity events to date. Importantly, no patients experienced non-hematologic adverse events as seen with many other compounds used to treat this patient population. Specifically, there were no reports of peripheral neuropathy, fatigue, cardiovascular events, or venous thromboembolisms. The efficacy and safety profile of CLR 131 shown to date allows future development of the compound, either at the Cohort 2 dose of 18.75 mCi/m2 or at one of the future higher doses being tested. The study is currently completing Cohort 3 at a single 25 mCi/m2 dose.
"ASH is a prestigious conference and this presentation represents a peer reviewed opportunity to report encouraging efficacy and safety data from our Phase I study of CLR 131 in relapsed/refractory multiple myeloma," said Jim Caruso, president and CEO of Cellectar Biosciences. "We look forward to reporting data from Cohort 3 at a single 25 mCi/m2 dose and the initiation of our NCI-sponsored Phase II trial in multiple myeloma and other hematologic malignancies."
The Phase I multi-center, open label, dose escalation study described in the poster outlines that CLR 131 was administered as a single dose, 30-minute intravenous infusion on Day 1 with a 40 mg oral dexamethasone dose weekly for 12 weeks. Each cohort consisted of five patients, of which four were evaluable (three men, one woman in Cohort 1 and two men, two women in Cohort 2). Patients in both cohorts received an average of 4 prior treatments. Half of all patients received a stem cell transplant. All patients received proteasome inhibitors and immunomodulatory drugs prior to enrollment as well as triple combination therapy at least once.
About CLR 131
CLR 131 is an investigational compound under development for a range of hematologic malignancies. It is currently being evaluated in a Phase I clinical trial in patients with relapsed or refractory multiple myeloma. The company plans to initiate a Phase II clinical study to assess efficacy in a range of B-cell malignancies in the first quarter of 2017. Based upon pre-clinical and interim Phase I study data, treatment with CLR 131 provides a novel approach to treating hematological diseases and may provide patients with therapeutic benefits, including overall response rate (ORR), an improvement in progression-free survival (PFS) and overall quality of life. CLR 131 utilizes the company’s patented PDC tumor targeting delivery platform to deliver a cytotoxic radioisotope, iodine-131 directly to tumor cells. The FDA has granted Cellectar an orphan drug designation for CLR 131 in the treatment of multiple myeloma.
About Phospholipid Drug Conjugates (PDCs)
Cellectar’s product candidates are built upon its patented cancer cell-targeting delivery and retention platform of optimized phospholipid ether-drug conjugates (PDCs). The company deliberately designed its phospholipid ether (PLE) carrier platform to be coupled with a variety of payloads to facilitate both therapeutic and diagnostic applications. The basis for selective tumor targeting of our PDC compounds lies in the differences between the plasma membranes of cancer cells compared to those of normal cells. Cancer cell membranes are highly enriched in lipid rafts, which are glycolipoprotein microdomains of the plasma membrane of cells that contain high concentrations of cholesterol and sphingolipids, and serve to organize cell surface and intracellular signaling molecules. PDCs have been tested in over 70 different xenograft models of cancer.
About Relapsed or Refractory Multiple Myeloma
Multiple myeloma is the second most common blood or hematologic cancer with approximately 30,000 new cases in the United States every year. It affects a specific type of blood cells known as plasma cells. Plasma cells are white blood cells that produce antibodies to help fight infections. While treatable for a time, multiple myeloma is incurable and almost all patients will relapse or the cancer will become resistant/refractory to current therapies.
Bio-Path Holdings Presents Clinical Data Evaluating BP1001 as a Treatment for Chronic Myelogenous Leukemia at the 58th Annual American Society of Hematology Annual Meeting
On December 5, 2016 Bio-Path Holdings, Inc., (NASDAQ: BPTH), a biotechnology company leveraging its proprietary DNAbilize liposomal delivery and antisense technology to develop a portfolio of targeted nucleic acid cancer drugs, reported that a review of BP1001 data as a treatment for chronic myelogenous leukemia (CML) was presented in a poster at the 58th Annual American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting taking place from December 3-6, 2016 in San Diego, CA (Filing, 8-K, Bio-Path Holdings, DEC 6, 2016, View Source [SID1234516978]).
Ana Tari Ashizawa, Ph.D., Bio-Path’s director of research, presented the poster titled "BP1001, a Novel Therapeutic for Chronic Myelogenous Leukemia." The results demonstrated that BP1001 decreased the proliferation of Gleevec (imatinib)-resistant CML cells in a dose-dependent manner. In addition, BP1001 pretreatment enhanced the inhibitory effects of Sprycel (dasatinib) in CML cells, leading to cell death. Five CML blast phase patients were enrolled in the first cohort (5 mg/m2 BP1001) of the Phase 1 BP1001 clinical study. Two CML patients, who had T315I mutation, showed significant reductions in circulating blasts during treatment. One patient’s blasts were reduced from 89% to 12%, while another patient’s blasts were reduced from 24% to 7%.
"These patient data, supported by previous in vivo and in vitro results, suggest that BP1001 has the potential to treat the 33% of CML patients who are resistant to Gleevec, the current standard of care. Sprycel is a second-generation tyrosine kinase inhibitor that is often used for Gleevec resistant patients. We are pleased that our preclinical results showed that BP1001 can enhance Sprycel activity in CML cells. These positive data give us confidence that BP1001 could play a valuable role in treating this patient population and encourage us to move forward with the initiation of our safety segment of the Phase 2 trial in patients with CML," said Peter Nielsen, chief executive officer of Bio-Path Holdings.
About BP1001
BP1001 (Liposomal Grb2 antisense) is Bio-Path’s lead product candidate, a neutral-charge, liposome-incorporated antisense drug designed to inhibit protein synthesis of Grb2 (growth factor receptor bound protein 2). Grb2 plays an essential role in cancer cell activation via the RAS pathway. Grb2 is an adapter protein that bridges signals between activated and mutated tyrosine kinases, such as Flt3, c-Kit, and Bcr-Abl, and the Ras pathway, leading to activation of the ERK and AKT proteins. Inhibition of Grb2 by BP1001 represents a significant advance in treating cancers with activated tyrosine kinases using a target not druggable with antibodies or kinase inhibitors. Inhibition of Grb2 has been demonstrated to halt cell proliferation and enhance cell killing by chemotherapeutic agents without added toxicity.
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