On April 18, 2016 Bellicum Pharmaceuticals, Inc. (Nasdaq:BLCM), a clinical stage biopharmaceutical company focused on discovering and developing novel cellular immunotherapies for cancers and orphan inherited blood disorders, reported that the Company, and its collaborating investigators at Leiden University Medical Center (LUMC), have been selected for a late-breaking poster presentation of a T cell receptor (TCR) product candidate containing the proprietary MyD88/CD40 activation switch (Go-TCR) at the AACR (Free AACR Whitepaper) 2016 Annual Meeting (Press release, Bellicum Pharmaceuticals, APR 18, 2016, View Source;p=RssLanding&cat=news&id=2157773 [SID:1234510961]). The conference will take place in New Orleans from April 16-20, 2016.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

The presentation, titled "Go-TCR: Inducible MyD88/CD40 (iMC) Enhances Proliferation and Survival of Tumor-Specific TCR-Modified T Cells, Increasing Anti-Tumor Efficacy" will highlight preclinical data demonstrating that its novel "go" switch can augment activation and expansion of TCR-engineered T cells while sensitizing tumors to T cells via cytokine-induced MHC class I upregulation.

The poster will be available in the Events & Presentations section of the Bellicum website at the time of the presentation.

Presentation Details

Abstract Number: LB-084
Presentation Title: "Go-TCR: Inducible MyD88/CD40 (iMC) Enhances Proliferation and Survival of Tumor-Specific TCR-Modified T cells, Increasing Anti-Tumor Efficacy"
Presentation Date: Monday, April 18, 2016
Presentation Time: 8:00 a.m. -12:00 p.m. CDT

On April 18, 2016 Heat Biologics, Inc. ("Heat") (Nasdaq:HTBX), an immuno-oncology company developing novel therapies that activate a patient’s immune system against cancer, reported that preclinical data from its collaboration with OncoSec Medical Incorporated ("OncoSec") focused on evaluating the combination of immunotherapy platforms were presented yesterday at the American Conference for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting (www.aacr.org) (Press release, Heat Biologics, APR 18, 2016, View Source [SID:1234510953]).

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

In the poster entitled "In vivo intra-tumoral electroporation of gp96-Ig/Fc-OX40L stimulates CD8+ T cell cross-priming to tumor specific neoantigens" (Abstract #567), researchers concluded that combining Heat’s ComPACT vaccine with OncoSec’s intratumoral DNA electroporation delivery platform stimulated an expansion of neoantigen-specific CD8+ T cells, leading to a regression in both treated and untreated cancer lesions in two mouse studies (melanoma and colorectal cancer). Heat and OncoSec announced their collaboration last year to evaluate the preclinical efficacy of delivering Heat’s immunotherapy vaccines via OncoSec’s ImmunoPulse platform.

"In this first preclinical study demonstrating the feasibility of electroporating ComPACT DNA plasmids, we saw robust neoantigen T cell response and tumor regression in both treated and untreated tumors, indicating a systemic anti-tumor response that could be reflective of what we might see in metastatic lesions," said Taylor Schreiber, M.D., Ph.D., Heat’s Chief Scientific Officer. "We believe that this approach is promising and that further studies are merited, especially as this combination approach has the potential to stimulate shared and private tumor antigens without introducing the complexities associated with personalized therapies."

"We are excited by our collaboration with Heat and by these initial findings. The ability of the tumor’s microenvironment to evade immune recognition and remain non-immunogenic is a significant challenge, which we believe needs to be addressed when designing new immuno-therapies," added Robert H. Pierce, M.D., OncoSec’s Chief Scientific Officer. "The initial feasibility data between our two platforms are encouraging and we are currently exploring the potential synergy between our platforms with both ComPACT and interleukin-12 expressing plasmids."

Copies of the abstract are available and can be viewed online through the AACR (Free AACR Whitepaper) website at www.aacr.org. The poster is available in the Publications section of Heat’s corporate website.

Codrituzumab, a humanized monoclonal antibody against Glypican-3 (GPC3) that is expressed in HCC, interacts with CD16/ FcγRIIIa and triggers antibody-dependent cytotoxicity. Codrituzumab was studied versus placebo in a randomized phase II trial in advanced HCC patients who had failed prior systemic therapy.
Patients with advanced HCC who had failed prior systemic therapy, ⩾18 years, ECOG 0-1, Child-Pugh A were randomized 2:1 to biweekly codrituzumab 1600 mg versus placebo. Patients were stratified based on GPC3 immunohistochemical expression: 2+/3+, 1+, and 0. Primary endpoint was progression free survival (PFS). Secondary endpoints include overall survival (OS), tolerability, pharmacokinetics (PK), and an exploratory endpoint in biomarkers analysis.
185 patients were enrolled: 125 received codrituzumab and 60 placebo: Median age 64/63, 85/75% male, 46/42% Asian, ECOG 0 65/63%, 74/77% having vascular invasion and/or extra-hepatic metastasis. 84%/70% had prior sorafenib. Drug exposure was 98.4% of planned dose, with an identical adverse events profile between the 2 groups. The median PFS and OS in the codrituzumab versus placebo groups in months were: 2.6 versus 1.5 (HR 0.97, P=0.87), and 8.7 versus 10 (HR 0.96, P=0.82). Projected Ctrough at cycle 3 day 1 based exposure, high CD16/FcγRIIIa on peripheral immune cells, and GPC3 expression in the tumor, were all associated with prolonged PFS and OS.
Codrituzumab did not show clinical benefit in this previously treated HCC population. Whether higher codrituzumab drug exposure or the use of CD16 and GPC3 as potential biomarkers would improve outcome remain unanswered questions.
Codrituzumab is a manufactured antibody against a liver cancer protein called glypican-3. In this clinical trial, codrituzumab was not found be effective against liver cancer. It was suggested though that a higher dose of codrituzumab or selecting patients with high level of glypican-3 or its mediator CD16 might improve outcome.
Copyright © 2016. Published by Elsevier B.V.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

The phase III MPACT trial in patients with metastatic pancreatic cancer (MPC) demonstrated superior efficacy of nab-paclitaxel (nab-P) plus gemcitabine (Gem) compared with Gem monotherapy, including the primary endpoint of overall survival (OS; median 8.7 vs. 6.6 months; hazard ratio [HR] 0.72; P < 0.001). A significant treatment difference favoring nab-P + Gem over Gem was observed for OS in patients treated in North America. The majority of patients were from the US (88%) with only 12% from Canada. Healthcare systems and treatment patterns are different between the 2 countries, and there is limited published information on outcomes of Canadian patients treated with first-line nab-P + Gem. This analysis evaluated efficacy and safety outcomes in Canadian patients in the MPACT trial.
Treatment-naive patients with MPC (N = 861) received either nab-P 125 mg/m(2) + Gem 1000 mg/m(2) on days 1, 8, and 15 every 4 weeks or Gem 1000 mg/m(2) weekly for the first 7 of 8 weeks (cycle 1) and then on days 1, 8, and 15 every 4 weeks (cycle ≥2).
The MPACT trial enrolled 63 patients in Canada. Baseline characteristics were well balanced and comparable with those of the intent-to-treat population. Both OS (median 11.9 vs. 7.1 months; HR 0.76; P = 0.373) and progression-free survival (median 7.2 vs. 5.2 months; HR 0.65; P = 0.224) were numerically longer and overall response rate (27% vs. 17%; P = 0.312) was numerically higher with nab-P + Gem vs. Gem. The most common grade ≥3 adverse events with nab-P + Gem vs. Gem were neutropenia (22% vs. 10%), fatigue (34% vs. 33%), and neuropathy (25% vs. 0%).
This subanalysis confirmed that nab-P + Gem is an efficacious treatment option and has a manageable safety profile in patients with MPC treated in Canada.
ClinicalTrials.gov identifier, NCT00844649.
Celgene Corporation, Summit, NJ, USA.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

The aim of this analysis was to establish the safety profile and tolerability of empagliflozin in patients with type 2 diabetes mellitus (T2DM) according to pooled data from several clinical trials.
Pooled data were analyzed from patients with T2DM treated with placebo (n = 3695), empagliflozin 10 mg (n = 3806), or empagliflozin 25 mg (n = 4782) in 17 randomized, Phase I, II, and III clinical trials plus 6 extension studies. Adverse events (AEs) were assessed descriptively in patients who took ≥1 dose of the study drug. AE incidence rates per 100 patient-years were calculated to adjust for differences in drug exposure across trials.
Total exposure was 3254, 3840, and 5649 patient-years in the placebo, empagliflozin 10 mg, and empagliflozin 25 mg groups, respectively. The incidence of any AEs, AEs leading to treatment discontinuation, severe AEs, and serious AEs was no higher in patients treated with empagliflozin than with placebo. Empagliflozin was not associated with an increased risk of hypoglycemia versus placebo, except in patients on background sulfonylurea and/or insulin. The incidence of events consistent with urinary tract infection was similar across treatment groups (9.4-11.3/100 patient-years); 0.4%, 0.2%, and 0.3% of patients in the placebo, empagliflozin 10 mg, and empagliflozin 25 mg groups, respectively, had urinary tract infections that required or prolonged hospitalization. The incidence of events consistent with genital infection was higher in patients treated with empagliflozin (4.7 and 5.0/100 patient-years for empagliflozin 10 and 25 mg, respectively) than placebo (1.3/100 patient-years), but only 0.1%, 0.1%, and <0.1% in the placebo, empagliflozin 10 mg, and empagliflozin 25 mg groups, respectively, had genital infections that required or prolonged hospitalization. The incidence of AEs consistent with volume depletion was similar with placebo, empagliflozin 10 mg, and empagliflozin 25 mg (1.6, 1.5, and 1.3/100 patient-years, respectively) and was higher with empagliflozin 25 mg than placebo or empagliflozin 10 mg in patients aged >75 years (4.4 vs 2.3 and 2.5/100 patient-years, respectively). The incidences of bone fractures, malignancies, decreased renal function, hepatic injury, venous thromboembolic events, and diabetic ketoacidosis were low and similar across the treatment groups.
In this predefined analysis that was based on >9000 patient-years’ exposure to empagliflozin, empagliflozin 10 mg, and empagliflozin 25 mg were well tolerated in patients with T2DM.
Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!