On April 11, 2018 Percans Oncology reported that it has developed i-CR, a personalized drug susceptibility testing platform for the precise treatment of colon cancer, to provide clinicians and patients with the most valuable medical plan for reference (Press release, Cothera Bioscience, APR 11, 2018, View Source [SID1234618854]).

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Features of i-CR in vitro drug susceptibility testing platform

i-CR drug susceptibility testing technology focuses on the functionality of tumor cells. It investigates the response of tumor cells under the action of drugs instead of exploring the relationship between drug susceptibility and changes in genes and proteins. The i-CR results are more practical and correspondence to clinical outcomes. This technology takes small samples of patients’ tumors, and performs rapid and high-throughput, drug susceptibility tests for drugs that have been marketed or entered clinical trials, thus providing a strong basis for clinicians to make optmized medical plans for each individual patient.

Target Patients

l Patients newly diagnosed as stage III or IV colorectal cancer;

l Patients who have failed the standard first-line treatment plan and hope to choose the best plan;

l Patients who have local or distant metastases and cannot benefit from genetic testing;

l Patients who are resistant to targeted drugs and need to find effective multiple targeted drugs and targeted combinations.

On April 11, 2018 Aileron Therapeutics (NASDAQ:ALRN), the clinical stage leader in the field of stapled peptide therapeutics for cancers and other diseases, reported the publication of nonclinical results in Science Translational Medicine demonstrating the anti-cancer potential of ALRN-6924 in models of Acute Myeloid Leukemia (AML) (Press release, Aileron Therapeutics, APR 11, 2018, View Source;p=RssLanding&cat=news&id=2342163 [SID1234525472]). ALRN-6924 is designed to reactivate p53-mediated tumor suppression by targeting the two primary p53 suppressor proteins, MDM2 and MDMX. ALRN-6924 is being evaluated in Phase 1 and Phase 2 clinical trials in patients with AML, myelodysplastic syndrome (MDS) and peripheral T-cell lymphoma (PTCL).

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In AML, blood-forming stem cells in the bone marrow produce abnormal red and white blood cells as a result of damage to DNA. P53, a natural tumor suppressor, is inactive in AML, allowing cancer cells to grow unimpeded. Reactivating p53 with ALRN-6924 appears to slow or stop the growth of both mature and immature cancer cells. As demonstrated by the researchers at Albert Einstein in their nonclinical studies, treatment with ALRN-6924 increased the median survival rate in an animal model of human AML (mice transplanted with human leukemia cells) from 50 to about 150 days. In addition, about 40% of the animals were cured, meaning they were tumor-free at one year.

"These data further support our belief that p53’s function may be more effectively restored when both MDMX and MDM2 are blocked. ALRN-6924, a stapled peptide therapeutic shown to inhibit both protein targets, has the potential to deliver on the long-held promise that restoring apoptosis through the p53 pathway may be critical in treating certain cancers," said Manuel Aivado, M.D., Ph.D., Chief Medical and Scientific Officer of Aileron.

"This is a very striking response. Most experimental drugs for leukemia in our experience achieve an increase in survival of only a few days in these preclinical models. Even more importantly, ALRN-6924 effectively cured about 40 percent of the treated mice," said study leader Ulrich Steidl, M.D., Ph.D., Professor of the Departments of Cell Biology and of Medicine and the Diane and Arthur B. Belfer Faculty Scholar in Cancer Research at Albert Einstein College of Medicine, and Associate Chair for Translational Research in Oncology at Montefiore.

The study in Science Translational Medicine is titled, "Dual inhibition of MDMX and MDM2 as a Therapeutic Strategy in Leukemia."

About ALRN-6924
ALRN-6924 is a first-in-class product candidate designed to reactivate wild type p53 tumor suppression by disrupting the interactions between the two primary p53 suppressor proteins, MDMX and MDM2. Aileron believes ALRN-6924 is the first and only product candidate in clinical development that can equipotently bind to and disrupt the interaction of MDMX and MDM2 with p53. Based on preclinical data and preliminary evidence of safety and anti-tumor activity in its ongoing clinical trials, there may be a significant opportunity to develop ALRN-6924 as a monotherapy or combination therapy for a wide variety of solid and liquid tumors. ALRN-6924 is currently being evaluated in multiple clinical trials for the treatment of acute myeloid leukemia (AML), advanced myelodysplastic syndrome (MDS) and peripheral T-cell lymphoma (PTCL). For information about its clinical trials, please visit www.clinicaltrials.gov.

On April 11, 2018 Cellectis (Euronext Growth: ALCLS – Nasdaq: CLLS), a clinical-stage biopharmaceutical company focused on developing immunotherapies based on gene-edited allogeneic CAR T-cells (UCART), reported that three posters regarding the Company’s allogeneic, off-the-shelf, CAR-T product candidates will be presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting to be held from April 14 to 18, 2018, in Chicago, Illinois (Press release, Cellectis, APR 11, 2018, View Source [SID1234525258]).

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April 16, 2018, 8:00 AM – 12:00 PM Central Time
Section 45

Repurposing endogenous immune pathways to improve chimeric antigen receptor T-cells potency
M. Sachdeva1, B. Busser1, S. Temburni1, A. Juillerat1, L. Poirot2, P. Duchateau2, J. Valton1;
1Cellectis, New York, NY, 2Cellectis, Paris, France

April 16, 2018, 1:00 PM – 5:00 PM Central Time
Section 24

Preclinical efficacy of allogeneic anti-CD123 CAR T-cells for the therapy of blastic plasmacytoid dendritic cell neoplasm (BPDCN)
T. Cai1, K. L. Black2, A. Naqvi2, R. Galetto3, A. Gouble3, J. Smith4, A. Cavazos1, L. Han1, Q. Zhang1, V. Kuruvilla1, S. N. Sergej Konoplev1, S. S. Neelapu1, A. A. Lane5, M. L. Guzman6, H. Kantarjian1, A. Thomas-Tikhonenko2, N. Pemmaraju1, M. Konopleva1;
1UT MD Anderson Cancer Ctr., Houston, TX, 2The Children’s Hosp. of Philadelphia, Philadelphia, PA, 3Cellectis SA, Paris, France, 4Cellectis Inc, New York, NY, 5Dana-Farber Cancer Inst., Boston, MA, 6Weill Cornell Med. Coll., New York, NY

April 18, 2018, 8:00 AM – 12:00 PM Central Time
Section 31

Prediction of immunotherapy outcome by multimodal assessment of minimal residual disease and persistence of allogeneic anti-CD123 CAR T-cells (UCART123) in pre-clinical models of acute myeloid leukemia
M. Sugita1, N. Mencia-Trinchant1, N. Ewing-Crystal1, G. Suppa1, R. Galetto2, A. Gouble2, J. Smith3, G. J. Roboz1, D. C. Hassane1, M. L. Guzman1;
1Weill Cornell Med., New York, NY, 2Cellectis SA, Paris, France, 3Cellectis Inc, New York, NY

Abstracts are available on the AACR (Free AACR Whitepaper) website. The three posters to be presented at the 2018 AACR (Free AACR Whitepaper) Annual Meeting will be available on the Cellectis website after April 18, 2018.

On April 11, 2018 Evotec AG reported a strategic collaboration with Petra Pharma Corporation ("Petra") (Press release, Evotec, APR 11, 2018, View Source;announcements/press-releases/p/evotec-forms-collaboration-with-petra-pharma-on-indigo-platform-5667 [SID1234525259]). Through the collaboration, Petra will access Evotec’s INDiGO platform to accelerate the development of its lead programme Petra-01, which is being developed for a range of oncological indications, through to the submission of an Investigational New Drug Application ("IND") with the U.S. Food and Drug Administration by the close of 2018. Evotec will leverage its highly skilled experts across all disciplines, primarily oncology, to implement a tailored drug development strategy for Petra-01 and will receive undisclosed research funding and success-based milestones.

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"Evotec has a strong track record of successful integrated development and INDiGO packages on behalf of their clients," said Brian O’Callaghan, President and Chief Executive Officer at Petra Pharma. "Our team at Petra is excited to progress our lead programme and look forward to achieving our goal to file an IND by the end of 2018. We are confident Evotec’s INDiGO programme and the team they assembled are the best partner to ensure the rapid and high-quality progression of Petra-01."

Dr Mario Polywka, Chief Operating Officer of Evotec, added: "Our INDiGO platform has proven to reduce the development time and cost of taking a pre-clinical candidate through to producing a quality data package for CTA and IND filings. Petra is a leader in the emerging NY life science ecosystem and we look forward to working with them long-term. We are excited for the opportunity to work with Petra on advancing its promising oncology candidate, Petra-01."

ABOUT PETRA-01
The lead program targets PIP4K2, an enzyme that phosphorylates PI(5)P (phosphoinositide 5 phosphate) to yield PI(4,5)P2 (phosphoinositide 4, 5, phosphate). Both substrate and product are important signaling molecules involved in regulation of cellular metabolism and growth. Published reports and Petra’s internal data support a role for inhibitors of PIP4K2 in selective killing of cancerous cells. This program has benefited from a highly productive collaboration with Sprint Biosciences, a leading fragment based drug discovery company.

On April 11, 2018 Acorda Therapeutics, Inc. (Nasdaq:ACOR) reported that it will host a conference call and webcast to report its first quarter 2018 financial results on Wednesday, May 2 at 8:30 a.m. ET (Press release, Acorda Therapeutics, APR 11, 2018, View Source [SID1234525262]).

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To participate in the conference call, please dial (833) 236-2756 (domestic) or (647) 689-4181 (international) and reference the access code 2477088. The presentation will be available on the Investors section of www.acorda.com.

A replay of the call will be available from 11:30 a.m. ET on May 2, 2018 until 11:59 p.m. ET on June 2, 2018. To access the replay, please dial (800) 585-8367 (domestic) or (416) 621-4642 (international); reference code 2477088. The archived webcast will be available in the Investor Relations section of the Acorda website at www.acorda.com.