On April 8, 2021 Vascular Biogenics Ltd. ("VBL Therapeutics" or the "Company") (NASDAQ: VBLT), reported that it intends to offer and sell ordinary shares and, to certain investors in lieu thereof, pre-funded warrants to purchase ordinary shares in an underwritten public offering (Press release, VBL Therapeutics, APR 8, 2021, View Source [SID1234577739]). As part of this proposed offering, VBL Therapeutics expects to grant the underwriters a 30-day option to purchase up to an additional 15% of the aggregate number of ordinary shares plus the ordinary shares underlying any pre-funded warrants that are sold in the offering, at the public offering price less the underwriting discounts and commissions. The offering is subject to market conditions, and there can be no assurance as to whether or when the offering may be completed, or as to the actual size or terms of the offering. All of the securities in the offering are to be sold by VBL Therapeutics.

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VBL Therapeutics intends to use the net proceeds from the offering for working capital and other general corporate purposes.

Guggenheim Securities, LLC is acting as bookrunning manager for the proposed offering. Oppenheimer & Co. Inc. is also acting as a joint bookrunner.

The securities described may be offered by VBL Therapeutics pursuant to a shelf registration statement on Form F-3 (No. 333-251821), including a base prospectus, previously filed with and declared effective by the Securities and Exchange Commission (the "SEC"). The securities may be offered only by means of a prospectus. A preliminary prospectus supplement relating to and describing the terms of the offering and a final prospectus supplement relating to and describing the terms of the offering will be filed with the SEC and will be available on the SEC’s website located at www.sec.gov. Copies of the preliminary prospectus supplement and the accompanying prospectus relating to the securities being offered may also be obtained by contacting Guggenheim Securities, LLC, Attention: Equity Syndicate Department, 330 Madison Avenue, 8th Floor, New York, New York 10017, by telephone at (212) 518-9544, or by email at [email protected].

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 jurisdiction in which such offer, solicitation or sale would be unlawful prior to the registration or qualification under the securities laws of any such jurisdiction.

On April 8, 2021 Varian (NYSE: VAR) reported it is collaborating with Google Cloud to build an advanced artificial intelligence (AI) based diagnostic platform to aid in the fight against cancer (Press release, Varian Medical Systems, APR 8, 2021, View Source [SID1234577738]). Varian and Google Cloud AI embarked on a deployment journey, using Neural Architecture Search (NAS) technology via Google Cloud AI Platform, to create AI models for organ segmentation—a crucial and labor-intensive step in radiation oncology that can be a bottleneck in the cancer treatment clinical workflow.

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Organ segmentation is the process of identifying the organs and tissues in diagnostic images that must be targeted or protected during a course of radiation therapy. These segmented images are then used to create radiotherapy treatment plans that specify where and how much dose will be deposited during treatment. This is a labor-intensive process that can take a clinician hours per patient. In some regions of the world, segmentation is a limiting factor in cancer patients’ access to advanced treatments like intensity-modulated radiotherapy (IMRT) that require accurate organ segmentation.

Varian is using Google Cloud AI Platform’s NAS technology to create an AI segmentation engine that is being "trained," using Varian’s proprietary treatment planning image data, to create customized auto-segmentation models for organs in the body. Varian intends to incorporate these models into its treatment planning software tools for use in cancer centers around the world.

"At Varian, we are working towards a world without fear of cancer, where high-quality cancer care—personalized and optimized for each patient—is available everywhere. To that end, we have committed ourselves to Intelligent Cancer Care, which seeks to automate routine or repetitive tasks in the radiation oncology workflow through the use of smart algorithms, machine learning, and AI," said Corey Zankowski, Senior Vice President, Technology and Innovation Office, Varian. "This collaboration with Google Cloud will turbocharge our efforts in this area."

"At Google Cloud, we believe AI technology has the power to impact a wide variety of industries, which is especially true in the field of medicine," said Craig Wiley, Director of Product Management, Google Cloud. "We are excited to see how Varian accelerates AI innovation and segmentation quality to improve cancer care with radiation therapy using our state-of-the-art NAS technology. As Varian’s AI platform of choice, our teams are working closely to deliver best-in-class AI for cancer treatment to patients around the world."

On April 8, 2021 Sutro Biopharma, Inc. (NASDAQ: STRO), a clinical-stage drug discovery, development and manufacturing company focused on the application of precise protein engineering and rational design to create next-generation cancer and autoimmune therapeutics, reported that Chief Executive Officer, Bill Newell, will present at two upcoming virtual investor conferences on April 15 and May 5, 2021 (Press release, Sutro Biopharma, APR 8, 2021, View Source [SID1234577737]).

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Presentation Details
20th Annual Needham Virtual Healthcare Conference

Date: Thursday, April 15, 2021

Presentation time: 2:15 p.m. ET / 11:15 a.m. PT

7th Annual Truist Securities Life Sciences Summit

Date: Wednesday, May 5, 2021

Presentation time: 1:50 p.m. ET / 10:50 a.m. PT

Live webcasts of each presentation can be accessed through the Events and Presentations page of the Investor Relations section on the company’s website at www.sutrobio.com. Archived replays of the webcasts will be available on the company’s website for approximately 30 days following each live presentation.

On April 8, 2021 Repare Therapeutics Inc. ("Repare" or the "Company") (Nasdaq: RPTX), a leading clinical-stage precision oncology company enabled by its proprietary synthetic lethality approach to the discovery and development of novel therapeutics, reported that it will host a virtual Investor Day webcast today from 10:30 a.m. – 12:00 p.m. ET, highlighting the progress of its proprietary RP-6306 program for tumors with genetic alterations characterized by CCNE1 amplification (Press release, Repare Therapeutics, APR 8, 2021, View Source [SID1234577736]). The Company expects to initiate a Phase 1 clinical trial of RP-6306 in the second quarter of 2021.

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"At today’s event, we will be reviewing the compelling pre-clinical anti-tumor activity of RP-6306, our first- in-class, selective, oral inhibitor of PKMYT1 to treat CCNE1-amplified, FBXW7-altered and other undisclosed PKMYT1 inhibitor-sensitive cancers. Our in vivo and other pre-clinical data indicate that RP-6306 can selectively inhibit tumors with these specific alterations when used as a monotherapy and in combination with other agents. We plan to initiate a Phase 1 clinical trial during this quarter, which is a quarter ahead of previously announced guidance," said Lloyd M. Segal, President and Chief Executive Officer of Repare. "We look forward to advancing our RP-6306 program into the clinic."

"There is a high unmet medical need for better treatments for patients with homologous recombinant-proficient cancers. The incidence of such cancers is rising and represents a growing therapeutic challenge." said Maria Koehler, MD, PhD, Chief Medical Officer of Repare. "Targeting DNA damage repair using synthetic lethal strategies is a massive opportunity to build on the success of PARP inhibitors. The field is rapidly expanding beyond PARP inhibitors and has been accelerated by the discovery of novel targets enabled by cancer genome sequencing and CRISPR technologies."

Highlights from the Virtual Investor Day

Pre-Clinical Data Findings

Using its proprietary, CRISPR-based SNIPRx discovery platform, Repare has identified PKMYT1 as a strong hit in a CCNE1-overexpression synthetic lethal screen. PKMYT1 is a kinase that phosphorylates CDK1, thereby holding the cyclin B-CDK1 complex in an inactive state until the cell is ready to enter mitosis. The Company’s product candidate RP-6306 is being developed as a highly potent and selective PKMYT1 inhibitor that preferentially kills tumor cells overexpressing CCNE1 and has shown to inhibit the growth of a broad range of CCNE1-amplified tumors in xenograft/PDX preclinical models, both as a single agent and in combination therapy settings. RP-6306 has been observed to have a favorable pre-clinical PK profile as well as low potential for drug-drug interactions. Application of Repare’s STEP2 genome-wide chemical screen has identified other gene alterations beyond CCNE1 amplification that are uniquely targetable by RP-6306, including tumors that have loss of FBXW7 function, a cell-cycle regulator that has been implicated as a key genetic driver in a broad range of cancers, and represent further areas of unmet medical need.

RP-6306 Phase 1 Clinical Trial Design

Repare plans to initiate enrollment of a Phase 1 clinical trial of RP-6306 during this quarter. Study objectives include assessment of safety, tolerability, dose and schedule (including the recommended Phase 2 dose). Subject to completion and review of the Phase 1 clinical trial, the Company expects to advance RP-6306, both as monotherapy and in combination with chemotherapies and other agents, into proof-of-concept studies in 2022 targeting a variety of patient populations, including those with tumors with CCNE1 amplification, FBXW7 loss or other undisclosed alterations identified through its proprietary STEP2 screen. Prospective enrichment of study patient populations will be guided by its ongoing efforts to develop patient selection biomarkers covering both target engagement and functional (DNA damage) readouts.

Virtual Investor Day Agenda

10:30 a.m. – 10:35 a.m. ET

Introduction

Lloyd Segal, President and Chief Executive Officer, Repare Therapeutics

10:35 a.m. – 10:50 a.m. ET

Targeting DNA Damage Repair in the Clinic

Timothy Yap, MBBS, Ph.D., FRCP

Medical Director, Institute for Applied Cancer Science, and Associate Professor, Department of Investigational Cancer Therapeutics, Division of Cancer Medicine at MD Anderson Cancer Center

10:50 a.m. – 11:05 a.m. ET

Genomic Classifications of Endometrial & Ovarian Cancers is Standard of Care

Unmet Need: Therapies Targeting CCNE1 & FBXW7

Carol Aghajanian, M.D.

Chief of Gynecologic Medical Oncology Service and Professor of Medicine, Weill Cornell Medical College, Memorial Sloan Kettering Cancer Center

11:05 a.m. – 11:35 a.m. ET

Target Discovery & Biology of RP-6306 & STEP Characterization Table

Michael Zinda, Ph.D., Executive Vice President, Chief Scientific Officer, Repare Therapeutics

11:35 a.m. – 11:45 a.m. ET

Translational & Clinical Plan for RP-6306

Maria Koehler, M.D., Ph.D., Executive Vice President, Chief Medical Officer, Repare Therapeutics

11:45 a.m. – 12:00 p.m. ET

Conclusion & Q&A Session

Conference Call and Webcast

To access the event virtual event, please dial (833) 638-9655 (U.S. and Canada) or (602) 585-9856 (international) at least 10 minutes prior to the start time and refer to conference ID 1093819. A live video webcast will be available in the Investor section of the Company’s website at View Source A webcast replay will also be available on the corporate website at the conclusion of the call.

About RP-6306

RP-6306, the result of Repare’s proprietary drug discovery program, is a first-in-class, selective, oral inhibitor of PKMYT1 to treat CCNE1-amplified, FBXW7-altered and other PKMYT1 inhibitor-sensitive cancers that typically do not respond well to platinum or PARP inhibitor treatment. Through Repare’s SNIPRx screen campaign for targets that are SL with CCNE1 amplification, the Company identified and validated this novel SL gene that has the characteristics of a therapeutic target. Subsequently, the Company developed novel and selective inhibitors against PKMYT1, which repeatedly demonstrated compelling anti-tumor activity, and announced the advancement of a clinical candidate for this first-in-class program. Repare anticipates initiating a Phase 1 clinical trial of RP-6306 during the quarter ending June 30, 2021. This trial is expected to enroll patients suffering from recurrent tumors characterized by CCNE1 amplification or other genomic alterations predicted to be sensitive to RP-6306. The primary objective of the trial is to assess preliminary safety in patients and to establish the RP2D and schedule for RP-6306 for further studies as a monotherapy. Dependent on Phase 1 result, an additional trial is planned to evaluate the combination of RP-6306 with approved anti-cancer agents, including chemotherapy.

On April 8, 2021 Onxeo S.A. (Euronext Growth Paris: ALONX, First North Copenhagen: ONXEO), ("Onxeo" or "the Company"), a clinical-stage biotechnology company specializing in the development of innovative drugs targeting tumor DNA Damage response (DDR), reported the presentation of preclinical data confirming the differentiated antitumoral properties of the drug candidates generated by platON, its patent-protected platform of decoy-agonists of the DNA Damage Response, in e-poster sessions during the American Association for Cancer Research (AACR) (Free AACR Whitepaper) (AACR 2021) virtual annual meeting on April 10, 2021 (Press release, Onxeo, APR 8, 2021, View Source [SID1234577735]).

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The first e-poster supports the ability of AsiDNA, the Company’s first-in-class DNA Damage Response (DDR) inhibitor, to prevent resistance to KRAS inhibitors (KRASi) emerging from drug-tolerant persister cells (DTC). Novel therapies targeting the inhibition of KRAS, an oncogenic protein present in a third of cancers, have shown very promising clinical results especially in non-small cell lung cancer. However, acquired resistance hinders their efficacy. Combining AsiDNA to KRASi could be an additional development opportunity for AsiDNA, in the context of its use to prevent acquired resistance to targeted therapies.

The second e-poster describes the mechanism of action of the molecules of the new OX400 family, specifically designed to interfere with PARP signaling and display immunomodulatory properties and metabolic effects.

Judith Greciet, Chief Executive Officer of Onxeo, commented: "Pharmaco-tolerant cells are a well-established cause of resistance to TKIs, and, as we already demonstrated last year, to PARP inhibitors. We have generated new data demonstrating that these cells are also involved in resistance to KRAS inhibitors and confirmed the efficacy of AsiDNA on these cells thus preventing or even reversing tumor regrowth. These results open the door for another potential combination with these innovative compounds which show high efficiency but struggle with resistance issues. In parallel, we continue to optimize the efficacy profile of the next candidates from the OX400 family, while keeping the established benefits shared by all our platON-sourced compounds in terms of safety and absence of resistance. Our new results confirm that, by trapping and exhausting specifically PARP, OX400 compounds have the potential to modulate the immune response and wear out the tumor cell metabolism. We will continue to explore these original properties."

Session: PO.ET03.05 – Reversal of Drug Resistance E-poster: 1433

Date/ Time: April 10, 2021 – 8:30 AM – 11:59 PM (U.S. Eastern Daylight Time -EDT)

To read the abstract: Acquired resistance to KRASG12C inhibitors evolves from drug-tolerant persister cells vulnerable to AsiDNA.

Recent progress has been made in the development of therapeutics against KRASG12C mutated tumors, which represent approximately 15% of lung adenocarcinoma. However, therapeutic resistance to KRASG12C inhibition is still a clinical hurdle. As we have previously shown with PARP inhibitors, we describe in these new data that resistance to KRASG12C inhibitors could also emerge, at least in part, from drug-tolerant persister cells, a specific cell population that undergo "dormancy" during treatment and accumulate mutations enabling the development of resistance to KRASG12C inhibitors. AsiDNA can target specifically this source of resistance and therefore prevents the emergence of acquired resistance to KRASG12C inhibitors, pointing to the therapeutic opportunity of combining AsiDNA and KRASG12C to overcome tumor progression or relapse.

Session: PO.CL06.07 – Immunomodulatory Agents and Interventions E-poster: 527

Date/ Time: April 10, 2021 – 8:30 AM – 11:59 PM (U.S. Eastern Daylight Time -EDT)

To read the abstract: A new generation of PARP interfering drug candidates for cancer treatment.

Onxeo pioneered a new approach of anti-cancer treatment to tackle acquired drug resistance: the decoy agonist mechanism of action. Drugs based on this mechanism hijack and hyperactivate therapeutic targets leading to an impairment of their physiological function. Our first compound using this breakthrough decoy agonist action, AsiDNA, has already shown target engagement, excellent safety profile in humans and importantly, lack of acquired resistance. We now describe the mechanism of action of our OX400 molecules, designed to trap PARP proteins. We show that these molecules, by interfering with PARP signaling, display immunomodulatory properties and metabolic effects. Our results provide a preclinical rationale for using OX400 molecules as immunomodulatory and "metabolic exhauster" agents, especially in appropriately molecularly selected patients with tumors showing metabolic deficiencies.