I-Mab to Participate at the 23rd Annual Needham Virtual Healthcare Conference

On April 5, 2024 I-Mab (NASDAQ: IMAB), a U.S.-based, global biotech company, exclusively focused on the development and potential commercialization of highly differentiated immunotherapies for the treatment of cancer, reported that management will present at the 23rd Annual Needham Virtual Healthcare Conference on April 11, 2024 (Press release, I-Mab Biopharma, APR 5, 2024, View Source [SID1234641824]).

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23rd Annual Needham Virtual Healthcare Conference

Presentation Time

Thursday, April 11 at 10:15 a.m. EST

Presenters

Raj Kannan, CEO; John Hayslip CMO

Webcast link

Here

Meetings

One-on-one and small group meetings: April 11, 2024

Management
Participants

Raj Kannan, CEO

Joe Skelton, CFO

John Hayslip, CMO
Tyler Ehler, Senior Director, Investor Relations

The webcast will also be available under "Event Calendar" on I-Mab’s IR website
at View Source

For more information, please contact your Needham representative.

Shasqi to Present Data on Novel Tumor-Targeted Drug Activation Technology at 2024 American Association for Cancer Research (AACR) Annual Meeting

On April 5, 2024 Shasqi, Inc. ("Shasqi"), a biotech company whose mission is to make cancer drugs more effective with click chemistry, reported it will present five posters on the company’s novel tumor-targeted drug activation approach at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting in San Diego, April 5-10, 2024 (Press release, Shasqi, APR 5, 2024, View Source [SID1234641823]).

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The posters will describe data generated with Shasqi’s CAPAC (Click Activated Protodrugs Against Cancer) approach. CAPAC uses 2022 Nobel Prize winning technology, click chemistry, to selectively activate high doses of cancer drugs directly at the tumor, minimizing toxicity to healthy cells and potentially improving the therapeutic index by dramatically altering the exposure. This approach overcomes many limitations of antibody-drug conjugates (ADCs).

"We are looking forward to sharing new data from the Shasqi pipeline at AACR (Free AACR Whitepaper)," said Shasqi Vice President of Research, Travis Biechele, Ph.D. "It is exciting to see data showing that we can effectively activate cancer drugs at the tumor using antigen-bound activators, resulting in sustained tumor regression."

Shasqi is advancing a pipeline of assets based on validated targets and payloads. The posters presented at the AACR (Free AACR Whitepaper) meeting will show preclinical efficacy and safety data for assets targeting HER2, TROP2, and NECTIN-4, each paired with either an MMAE or exatecan payload.

Presentations
Abstracts are available and can be viewed on the AACR (Free AACR Whitepaper) website.

Monday, April 8 between 9 AM – 12:30 PM PST

Click chemistry enabled selective activation of highly cytotoxic MMAE payload at tumors using TROP2 targeting agent

Lead Author: George Coricor, Ph.D.
Poster Section 28, Poster Board: 13
Wednesday, April 10 between 9 AM – 12:30 PM PST

Tumor targeted activation of an attenuated exatecan protodrug through Click Chemistry demonstrates efficacy in murine tumor studies

Lead Author: Sangeetha Srinivasan, Ph.D.
Poster Section 26, Poster Board: 1
A click chemistry-based HER2 targeting agent activates a decoupled MMAE payload making it highly differentiated in efficacy and safety than ADCs

Lead Author: Sangeetha Srinivasan, Ph.D.
Poster Section 26, Poster Board: 2
Nectin-4 targeted therapy with MMAE protodrug results in anti-tumor efficacy mediated by click chemistry

Lead Author: George Coricor, Ph.D.
Poster Section 26, Poster Board: 3
Improving anti-tumor efficacy by modulating a separate HER2 activator and an MMAE payload and reuniting both through click chemistry

Lead Author: Stefanie Wagner
Poster Section 26, Poster Board: 4

Precision Biologics to Present at the American Association for Cancer Research (AACR) Annual Meeting on April 8th, 2024

On April 5, 2024 Precision Biologics, Inc. reported its lead monoclonal antibody, NEO-201, targets circulating human naïve regulatory T cells (Tregs) in both healthy donors and cancer patients (Press release, Precision Biologics, APR 5, 2024, View Source [SID1234641822]). A poster presentation discussing this data will be presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2024, at the San Diego Convention Center in San Diego, CA on April 8th, 2024.

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Poster title: The O-glycan epitope targeting anti-human carcinoma monoclonal antibody (mAb) NEO-201 can also target human regulatory T cells (Tregs)

This study was performed by Drs. Atsushi Tanaka and Shimon Sakaguchi from Osaka University, Japan. Dr. Sakaguchi’s group independently analyzed by flow cytometry the ability of NEO-201 to recognize naïve Tregs in peripheral blood mononuclear cells (PBMCs) from healthy donors, confirming findings from Precision Biologics in PBMCs from cancer patients.

Previous studies performed by Precision Biologics have shown that approximately 4.6% of CD4+ T cells express NEO-201 target antigen and that those CD4+ T cells have Tregs phenotype. In addition, in a recently published phase 1 clinical study it has been observed that NEO-201 binds to CD4+/ CD25+/, CD127-/, Foxp3+/, CD15s+ cells from PBMCs from cancer patients with solid tumors. The purpose of this study performed in Dr. Sakaguchi’s laboratory was to corroborate and further characterize the phenotype of the specific subset of CD4+ T cells expressing the NEO-201 target antigen.

In this study, human PBMCs were collected from 7 healthy donors (HD) at Osaka University and 6 cancer patients from Precision Biologics ongoing phase II clinical trial (Clinical Trial NCT03476681) evaluating the efficacy of the combination of NEO-201 with pembrolizumab in adults with solid tumors resistant to checkpoint inhibitors. Phenotypic analysis was conducted by flow cytometry to evaluate which fraction of CD4+ T cells is recognized by NEO-201.

Flow cytometry analysis revealed that NEO-201 recognizes fraction I of CD4 T cells in both healthy donors and cancer patients. Fraction I includes naïve Tregs (nTregs) with the following phenotype: CD3+/CD4+/CD45RA+/Foxp3low cells. The percentage of nTregs in cancer patients was higher than the percentage detected in healthy donors. On the other hand, this study revealed that NEO-201 does not bind to fraction II of CD4 T cells in both healthy donors and cancer patients. Fraction II includes effector Tregs (eTregs) with the following phenotype: CD3+/CD4+/CD45RA-/Foxp3high cells.

When subjected to t-cell receptor (TCR) stimulation, nTregs undergo proliferation and differentiate into eTregs, which can then infiltrate into tumor microenvironment (TME) and induce suppression of anticancer immunity.

Depletion of circulating NEO-201 positive nTregs in cancer patients after NEO-201 treatment may prevent the differentiation of nTregs into eTregs, thus reducing their accumulation in the TME. This study suggests therapy with NEO-201 may reduce Treg-mediated suppression of anticancer immunity.

The poster will be presented in person at the San Diego Convention Center, San Diego, CA, on Monday April 8th, 2024. Please stop by poster # 2716 at Poster Section 6, Poster Board number 7 (1.30 p.m.–5.00 p.m.).

BOLD-100 and ATR Inhibitors as a New Avenue for PDAC Targeting at AACR 2024

On April 5, 2024 Bold Therapeutics, a clinical-stage biopharmaceutical company at the forefront of developing innovative metallotherapeutics, reported that Dr. Do-Youn Oh’s group at Seoul National University College of Medicine, Seoul, South Korea, will be presenting at the AACR (Free AACR Whitepaper) Annual Meeting, April 5-10, 2024, in San Diego, California on the use of BOLD-100 in combination with ATR (Ataxia telangiectasia and Rad3-related protein serine/threonine kinase) inhibitors as anticancer therapies for the treatment of Pancreatic Ductal Adenocarcinoma (PDAC) (Press release, Bold Therapeutics, APR 5, 2024, View Source [SID1234641821]).

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Bold Therapeutics’ BOLD-100, a pioneering ruthenium-based small molecule, uniquely acts by (1) targeting GRP78 to modulate the unfolded protein response (UPR) and (2) generating reactive oxygen species (ROS) leading to DNA damage and cell cycle arrest. This dual action triggers cell death across a spectrum of cancer types, including those resistant to current treatments. As a result, BOLD-100 holds promise for significantly enhancing treatment outcomes in a diverse array of both solid and liquid tumors when used alongside a broad range of anticancer treatments, from conventional chemotherapies to cutting-edge targeted therapies and immuno-oncology agents. Our recent presentation at ASCO (Free ASCO Whitepaper) GI 2024 showcased positive Phase 2 clinical trial results in the treatment of advanced metastatic colorectal cancer (mCRC) in patients previously treated with FOLFOX / CAPOX. The data, highlighting patients treated with a combination of BOLD-100 and FOLFOX, demonstrated notable safety and clinical improvements, bolstering confidence in the therapeutic value of BOLD-100.

Dr. Do-Youn Oh’s group at Seoul National University College of Medicine, South Korea will be presenting a poster entitled, "Co-downregulation of GRP78 and ATR enhances apoptosis in pancreatic ductal adenocarcinoma," (Poster no. 12, Session: Cellular Stress Responses 1). This work underscores the significant impact of BOLD-100 in inducing GRP78 inhibition, which substantially triggers oxidative stress. Furthermore, when combined with ATR inhibition, this synergy effectively promotes cell death.

Key Findings:

BOLD-100 elevates ER stress and ROS, leading to activation of the UPR pathway and CHOP-dependent apoptosis, which inhibits PDAC growth;
ROS accumulation activates the ATR-CHK1 DNA damage repair pathway, which NAC can abrogate; and
The combination of BOLD-100 with the ATR inhibitor AZD6738 exhibits a synergistic effect, suggesting GRP78/ATR dual targeting as a promising therapeutic approach for PDAC.
These findings unveil a compelling strategy for combinational targeting to inhibit PDAC growth.

"DNA repair mechanisms play a crucial role in maintaining genomic integrity, leading to cell cycle arrest and thereby preventing the uncontrolled growth and progression of cancer cells. Our in-vitro and in-vivo findings indicate that combining BOLD-100 with ATR inhibition results in synthetic lethality against highly aggressive Pancreatic Ductal Adenocarcinoma. We are eager to delve deeper into this research path and its potential clinical utility," stated Dr. Oh.

Mark Bazett, Sr Director, Preclinical Development at Bold Therapeutics added, "BOLD-100 has already demonstrated remarkable safety and efficacy in the treatment of metastatic colorectal cancer (mCRC). Diverging from the path of targeted therapies, BOLD-100’s unique multi-modal mechanism-of-action opens avenues for potent combination therapies designed to tackle some of the most difficult-to-treat cancers including those resistant to standard treatments. The synergistic combination identified by Dr. Oh’s group holds particular promise, and we look forward to further exploring this potential."

Jim Pankovich, EVP, Clinical Development at Bold Therapeutics, and Mark Bazett, Sr Director, Preclinical Development at Bold Therapeutics, will also be attending the 2024 AACR (Free AACR Whitepaper) Annual Meeting in San Diego and are available for in-person discussions related to BOLD-100.

For additional details, visit Bold Therapeutics’ website at www.bold-therapeutics.com or the AACR (Free AACR Whitepaper) conference site at View Source

Antengene Presents Four Preclinical Posters at AACR 2024

On April 5, 2024 Antengene Corporation Limited ("Antengene", SEHK: 6996.HK), a leading innovative, commercial-stage global biopharmaceutical company dedicated to discovering, developing and commercializing first-in-class and/or best-in-class medicines for cancer, reported the presentation of four preclinical posters at the 2024 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting (AACR 2024), taking place from April 5th to April 10th at the San Diego Convention Center in San Diego, California, the United States (Press release, Antengene, APR 5, 2024, View Source [SID1234641820]). The posters showcased four of Antengene’s high-potential emerging programs, including ATG-042, tracking to a H1 2025 IND filing; ATG-022, in Phase II dose expansion studies in China and Australia; AnTenGagerTM platform, Antengene’s proprietary T-cell engager (TCE) platform; and ATG-102, which could be the first IND candidate from AnTenGagerTM platform.

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ATG-042, an oral small molecule MTAPnull-selective PRMT5 inhibitor holding the promise as a best-in-class drug. Study results showed that ATG-042 has the potential to elegantly target tumor cells while sparing healthy cells, with an attractive developability profile. ATG-022 is an Claudin 18.2 antibody-drug conjugate. The detailed updated data of the Claudin 18.2 (CLDN18.2) companion diagnostic antibody candidate for ATG-022 showed that the antibody has higher sensitivity compared to commercially available kits. AnTenGagerTM, Antengene’s proprietary TCE platform with the ability to induce target-dependent T-cell activation, has potent anti-tumor effects and lower risk of cytokine release syndrome (CRS). ATG-102, a LILRB4 x CD3 TCE, is being developed for the treatment of acute myeloid leukemia (AML).

Details of the posters:

ATG-042 (MTAPnull-selective PRMT5 Inhibitor)

Title: Preclinical characterization of ATG-042, a novel MTAPnull-selective PRMT5 inhibitor

Abstract: 4592

Session Category: Experimental and Molecular Therapeutics

Session Title: HDAC and Methyltransferase Inhibitors

Date: April 9, 2024

Time: 9:00 AM – 12:30 PM (Pacific Time)

12:00 AM – 3:30 AM, April 10, 2024 (Beijing Time)

Location: Poster Section 24

This preclinical study was designed to test the in vitro/in vivo efficacy, and preclinical pharmacokinetic (PK) properties of ATG-042.
According to the results, ATG-042 demonstrated a potent and selective inhibitory effect on the proliferation of MTAP knockout cells, showed high permeability, good metabolic stability, a low risk of drug-drug interaction (DDI), and high oral bioavailability. Importantly, ATG-042 demonstrated good brain penetrability. In CDX models, ATG-042 also potently and selectively inhibited tumor growth without inducing weight loss.
These data suggest that ATG-042 is an orally administered, MTAPnull-selective PRMT5 inhibitor with potent efficacy against MTAP-null tumors, as well as demonstrating good tolerability and favorable preclinical PK profiles.
Companion Diagnostic Antibody for ATG-022 (Claudin 18.2 ADC)

Title: Development of a novel companion diagnostic immunohistochemistry antibody for Claudin 18.2-targeted therapies

Abstract: 1032

Session Category: Clinical Research

Session Title: Diagnostic Biomarkers 1

Date: April 7, 2024

Time: 1:30 PM – 5:00 PM (Pacific Time)

4:30 AM – 8:00 AM, April 8, 2024 (Beijing Time)

Location: Poster Section 42

Despite the substantial correlation between the expression of CLDN18.2 and the efficacy of therapies targeting CLDN18.2, no companion diagnostic (CDx) antibodies specific to CLDN18.2 have been approved to date. This poster presents the discovery and validation of a novel, highly sensitive immunohistochemistry (IHC) antibody that selectively identifies CLDN18.2.
According these data, the monoclonal antibody (mAb) clone 43F11 showed positive cell surface IHC staining on CLDN18.2-expressing cells following fixation but demonstrated no staining on CLDN18.1-expressing cells. Moreover, the 43F11 antibody accurately identified the expression level of CLDN18.2 in an IHC assay, utilizing tumor tissues and patient-derived xenograft (PDX) samples with predetermined expression levels of CLDN18.2. When compared to the commercially available IHC antibody EPR19202, the 43F11 antibody demonstrated greater sensitivity, enabling positive staining on cancer tissues with significantly lower expression levels of CLDN18.2.
These data suggest that the 43F11 antibody possesses superior sensitivity compared to the benchmark antibody and has the potential to serve as an effective patient stratification tool.
AnTenGagerTM Platform

Title: AnTenGagerTM, a novel "2+1" T cell engager platform, enables conditional T cell activation with reduced risk of CRS

Abstract: 6343

Session Category: Clinical Research

Session Title: Antibodies 2

Date: April 9, 2024

Time: 1:30 PM – 5:00 PM (Pacific Time)

4:30 AM – 8:00 AM, April 10, 2024 (Beijing Time)

Location: Poster Section 41

This poster presents an in-depth overview of the design and mechanism of action for the proprietary AnTenGagerTM T cell engager (TCE) platform. These TCEs are specifically designed to produce an anti-cancer effect with a lower risk of systemic CD3 activation and cytokine release syndrome (CRS), potentially paving the way for use in solid tumors.
AnTenGagers TCE constructs are designed to induce cytotoxicity by forming a T cell receptor (TCR)-independent immune synapse. AnTenGagers do this by simultaneously binding tumor associated antigens (TAAs) on cancer cells and specific conformational epitopes on CD3+ T-cells.
Presented data show that AnTenGagers are able to effectively bind to specific CD3 confirmational epitopes and demonstrate higher cytotoxicity compared to benchmark compounds.
AnTenGagers are compatible with a range of TAAs, and that AnTenGagers have improved cytotoxicity compared to benchmark compounds, as demonstrated in cellular assays and a murine myeloma model. Data from the murine models also showed that AnTenGagers resulted in significantly lower concentrations of pro-inflammatory cytokines, further supporting a lower risk of CRS.
AnTenGagers also have good "developability" properties based on good stability under stress conditions.
Together, these data support the potential for AnTenGagers to be used in solid tumors, based on their ability to simultaneously bind TAAs and specific CD3+ confirmational epitopes, resulting in higher TAA-dependent cytotoxicity compared to benchmarks and the reduced risk of CRS, opening the door to a broad new class of cancer therapies.
ATG-102 (LILRB4 x CD3 T Cell Engager)

Title: ATG-102, a novel LILRB4 x CD3 T cell engager, targeting two non-overlapping epitopes of LILRB4, for the treatment of monocytic AML

Abstract: 2372

Session Category: Clinical Research

Session Title: Antibodies 1

Date: April 8, 2024

Time: 9:00 AM – 12:30 PM (Pacific Time)

12:00 AM – 3:30 AM, April 9, 2024 (Beijing Time)

Location: Poster Section 38

The use of TCEs to treat AML (acute myeloid leukemia) has been limited the difficulty in identifying specific antigens that are expressed on AML and leukemic stem cells but not normal hematopoietic stem cells. The preferential expression of LILRB4 on M4/M5 subtype acute myeloid leukemia (AML) cells renders it a highly attractive target for the treatment of AML. These data show that an AnTenGagerTM based TCE, which binds to two distinct epitopes of the LILRB4 receptor, can induce potent T-cell dependent cellular cytotoxicity (TDCC) to produce potent anti-tumor efficacy in vitro and in vivo.
The poster outlines the design and structural characteristics of ATG-102 comprised of two LILRB4 epitopes and an anti-CD3 single chain fragment variable (scFv) inserted in the hinge region on one of the LILRB4 heavy chains. Characterization data include:
-Binding epitope and affinity studies showing that ATG-102 binds to the target TAA epitopes as well as conformational CD3 epitopes.
-T cell binding and T-cell dependent cytotoxicity assays show that compared to the benchmark, ATG-102 demonstrated less non-specific T cell binding or activation, whilst inducing more potent TDCC against LILRB4+cells and enhanced in vivo anti-AML efficacy.

These data highlight the structural characteristics of ATG-102 and demonstrate potent in vitro and in vivo anti-tumor efficacy which support further clinical evaluation of ATG-102.