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61st ASH Congress 2019: Menarini Ricerche Presents the Latest Updates About the First In Human Clinical Trial of SEL24/MEN1703

On December 9, 2019 Menarini Ricerche reported is progressing with the clinical development of SEL24/MEN1703, and will be presenting the design of the ongoing First In Human clinical trial DIAMOND-01 (NCT03008187) at the 61st ASH (Free ASH Whitepaper) Congress, with a poster entitled: "First in Human Study of SEL24/MEN1703, First in Class, Orally Available Dual PIM/FLT3 Kinase Inhibitor, in Patients with Acute Myeloid Leukemia (Press release, Menarini, DEC 9, 2019, View Source [SID1234552165])." The poster, which will be disclosed today during the "Acute Myeloid Leukemia: Novel Therapy, excluding Transplantation" session, describes the ongoing adjustment to the dose escalation design, with the objective to obtain more robust data on the recommended phase 2 dose.

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CLI24-001 (DIAMOND-01) trial is testing SEL24/MEN1703, a first in class, oral dual PIM/FLT3 inhibitor in-licensed from Ryvu Therapeutics. The primary objective of the study, currently carried out in newly diagnosed, relapsed or refractory AML (excluding acute promyelocytic leukemia) patients who are unsuitable for intensive chemotherapy, is to identify the recommended phase 2 dose of SEL24/MEN1703 given as single agent.

Furthermore, a second abstract reporting the identification of a pharmacodynamic biomarker for SEL24/MEN1703 and its implementation in the DIAMOND-01 trial, has been disclosed by ASH (Free ASH Whitepaper) as e-publication and is available in a special online-only issue of ASH (Free ASH Whitepaper)’s official Journal -Blood (2019) 134 (Supplement 1): 5087-.

Menarini strongly believes in innovation and is investing in the research and development of new treatment options for oncology patients, focusing on targeted therapies and precision medicine approaches. The contribution of Menarini Ricerche to ASH (Free ASH Whitepaper) with these data confirms such commitment to the development of innovative drugs that meet the needs of patients with difficult to treat cancers and poor prognosis.

CNS Pharmaceuticals to Participate in the 8th Annual ROTH Deer Valley Corporate Access Event

On December 9, 2019 CNS Pharmaceuticals, Inc. (NASDAQ: CNSP) ("CNS" or the "Company"), a biotechnology company specializing in the development of novel treatments for brain tumors, reported that John Climaco, Chief Executive Officer of CNS Pharmaceuticals, and Chris Downs, Chief Financial Officer, will be attending the 8th Annual ROTH Deer Valley Corporate Access Event at the Montage Deer Valley Hotel in Park City, Utah (Press release, CNS Pharmaceuticals, DEC 9, 2019, View Source [SID1234552164]).

Event:

8th Annual ROTH Deer Valley Corporate Access Event

Format:

Small Group & 1×1 Meetings

Date:

December 11-12, 2019

Location:

Montage Deer Valley Hotel, Park City, Utah

About Berubicin
Berubicin is an anthracycline, a class of drugs among the most powerful chemotherapy drugs and effective against more types of cancer than any other class of chemotherapeutic agents. Anthracyclines are designed to damage the DNA of targeted cancer cells by interfering with the action of the topoisomerase II, a critical enzyme enabling cell proliferation. Berubicin was developed at the MD Anderson Cancer Center (MDACC), the world’s largest cancer research facility. Berubicin appeared to demonstrate one Durable Complete Response in a Phase I human clinical trial conducted by a prior developer.

Biocept Announces Pricing of $10.0 Million Underwritten Public Offering

On December 9, 2019 Biocept, Inc. (NASDAQ: BIOC) ("Biocept" or the "Company"), a leading commercial provider of liquid biopsy solutions, reported the pricing of an underwritten public offering of 24,600,000 shares of its common stock (or pre-funded warrants to purchase common stock in lieu thereof) and warrants to purchase up to 24,600,000 shares of the Company’s common stock (Press release, Biocept, DEC 9, 2019, View Source [SID1234552163]). Each share of common stock or pre-funded warrant is being sold together with one warrant to purchase one share of common stock at a combined price to the public of $0.405 per share and warrant. Gross proceeds, before underwriting discounts and commissions and estimated offering expenses, are expected to be approximately $10.0 million.

The warrants will be immediately exercisable at a price of $0.405 per share of common stock and will expire five years from the date of issuance. Additionally, if the volume-weighted average price of our common stock is below the exercise price per share of the warrants on any trading day beginning the earlier of (i) 30 days from today, and (ii) the trading day on which the aggregate trading volume of our common stock is equal to more than three times the number of shares of common stock sold in the offering, then the warrantholders may elect to cashless exercise their warrants for a number of shares equal to 50% of the shares issuable upon cash exercise. Each pre-funded warrant has an exercise price of $0.01 per share, is exercisable immediately and will expire when exercised in full. The shares of common stock or the pre-funded warrants and the accompanying warrants, can only be purchased together in the offering, but will be issued separately and will be immediately separable upon issuance. The offering is expected to close on or about December 11, 2019, subject to customary closing conditions.

Maxim Group LLC is acting as the book-running manager and Dawson James Securities, Inc. is acting as a co-manager in connection with the offering.

Biocept also has granted to Maxim Group LLC a 45-day option to purchase up to an additional 3,690,000 shares of common stock and/or warrants to purchase up to 3,690,000 shares of common stock, at the public offering price less discounts and commissions.

The offering is being conducted pursuant to the Company’s registration statement on Form S-1 (File No. 333-234459), as amended, previously filed with and subsequently declared effective by the Securities and Exchange Commission ("SEC"). A final prospectus relating to the offering will be filed with the SEC and will be available on the SEC’s website at View Source Electronic copies of the final prospectus relating to this offering, when available, may be obtained from Maxim Group LLC, 405 Lexington Avenue, 2nd Floor, New York, NY 10174, at (212) 895-3745.

This press release shall not constitute an offer to sell or the solicitation of an offer to buy these securities, nor shall there be any sale of these securities in any state or other jurisdiction in which such offer, solicitation or sale would be unlawful prior to the registration or qualification under the securities laws of any such state or other jurisdiction.

Samus Therapeutics Announces Presentation of Phase 1b Study Evaluating Orally Administered PU-H71 with Ruxolitinib in Myelofibrosis at the ASH 2019 Annual Meeting

On December 9, 2019 Samus Therapeutics, Inc. ("Samus" or the "Company"), a privately held, Boston-based, biopharmaceutical company developing epichaperome inhibitors to intervene in pathological processes and initiate the degradation of disease-associated proteins, reported a poster presentation addressing the Company’s Phase 1 study evaluating orally administered PU-H71 with ruxolitinib in patients with myelofibrosis no longer fully responsive to orally administered ruxolitinib (Press release, Samus Therapeutics, DEC 9, 2019, View Source [SID1234552162]). The poster is being presented today at the American Society of Hematology (ASH) (Free ASH Whitepaper) 2019 Annual Meeting in Orlando.

"Preclinical data show us that the activity of mutated JAK2 is tightly regulated by epichaperomes, a complex network of proteins which forms under cellular stress, such as in cancer, and nucleates on heat shock protein 90," commented Barbara Wallner, Chief Scientific Officer of Samus Therapeutics. "PU-H71 offers a novel approach to address frontline treatment of myelofibrosis in combination to potentially improve outcomes."

The combination multicenter Phase 1b study is designed to assess the safety, tolerability, pharmacodynamics, and preliminary efficacy of orally administered PU-H71 in myelofibrosis, for which the U.S. Food and Drug Administration granted Orphan Drug designation in 2018. The study will enroll patients who have active disease and have been receiving ruxolitinib therapy for at least 3 months. The study employs a standard 3+3 dose escalation design beginning with 50 mg/day of PU-H71 to determine the maximum tolerated dose (MTD). Enrollment in the study is now ongoing in the United States.

"Early study of intravenously administered PU-H71 in myelofibrosis in combination with ruxolitinib identified a safe and tolerable dose and we redirected our efforts to oral administration," said Dick Bagley, President and Interim Chief Executive Officer of Samus Therapeutics. "We believe that the combination of PU-H71 and ruxolitinib could deliver added clinical benefit in this extraordinarily difficult to treat hematological malignancy."

Details for the ASH (Free ASH Whitepaper) 2019 presentation are as follows:

Title: Phase 1b Study of the Epichaperome Inhibitor PU-H71 Administered Orally with Ruxolitinib Continuation for the Treatment of Patients with Myelofibrosis
Lead author: Dr. Naveen Pemmaraju, Associate Professor, Department of Leukemia, MD Anderson Cancer Center
Paper #: 4178
Session: 634. Myeloproliferative Syndromes: Clinical: Poster III
Date and Time: Monday, December 9, 2019; 6:00 PM-8:00 PM ET
Location: Orange County Convention Center, Hall B

Kymera Therapeutics to Present Preclinical Data Demonstrating Potent Antitumor Activity by a Selective STAT3 Degrader in Hematologic Malignancies at the American Society of Hematology Annual Meeting

On December 9, 2019 Kymera Therapeutics Inc., a biotechnology company pioneering targeted protein degradation to discover breakthrough medicines for patients, reported the company will present new preclinical data showing the further characterization of novel, highly selective and potent degraders of STAT3 with activity across multiple hematologic malignancies including ALK-positive anaplastic large cell lymphoma (ALK+ ALCL), acute myelogenous leukemia (AML) and diffuse large B cell lymphoma (DLBCL) (Press release, Kymera Therapeutics, DEC 9, 2019, View Source [SID1234552161]). Data will be shared during a poster presentation (Abstract #3803) at the American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting in Orlando on Monday, Dec. 9 at 6:00 PM EST in Orange County Convention Center, Hall B, Level 2.

STAT3 is an oncogenic transcription factor downstream of multiple signaling events including the IL-6/JAK and ALK pathways. Activating mutations and aberrant activation of STAT3 drive a subset of tumors via induction of autocrine factors that promote tumor proliferation and survival, as well as induction of proteins that contribute to a tumor permissive microenvironment. Degrading STAT3 has been shown to disrupt downstream signaling and induce antitumor responses in STAT3-dependent hematologic malignancies.

"As Kymera advances our STAT3 degraders into the clinic, we continue to expand the characterization of the biological impact of STAT3 degradation in liquid and solid tumors including the pharmacodynamic effect required to achieve complete tumor regression in a mouse xenograft model of ALK+ ALCL," said Jared Gollob, MD, CMO of Kymera Therapeutics. "These data highlight the potential for STAT3 degraders to treat STAT3-dependent lymphomas and leukemias, and enable the rational development of a treatment regimen that maximizes the probability of success in patients. We plan to select a lead STAT3 degrader for IND-enabling studies in 2020."

ASH Study Highlights
ABSTRACT #3803, "Small Molecule-Induced, Selective STAT3 Degradation Leads to Anti-Tumor Activity in STAT3-Dependent Heme Malignancies," presented by Fred Csibi, PhD, Associate Director, Oncology Biology at Kymera Therapeutics.

KYM-003 treatment resulted in rapid, potent and highly selective STAT3 degradation with similar activity against both mutant and wild-type STAT3.
KYM-003 repressed the growth in vitro of multiple ALK+ ALCL cell lines as well as AML and DLBCL.
Sustained STAT3 degradation of 90% or greater led to apoptosis induction and cancer cell death within 48hr in vitro and in vivo.
Intermittent dosing of KYM-003 achieved complete tumor regression in an ALK+ ALCL mouse xenograft model.