On March 25, 2025 CStone reported that it will showcase its latest preclinical studies on five internally developed innovative candidates, including the trispecific antibody CS2009, the bispecific antibody CS2011, and three novel antibody-drug conjugates (ADCs) developed from CStone’s proprietary ADC platform: CS5006, CS5007, and CS5005 (Press release, CStone Pharmaceauticals, MAR 25, 2025, View Source [SID1234651423]). The abstracts will be published in Cancer Research, the official journal of AACR (Free AACR Whitepaper), on April 11 (ET).

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CS2009 is a trispecific antibody targeting PD-1, VEGFA, and CTLA-4. Its innovative molecular design is expected to enhance anti-tumor efficacy by preferentially targeting PD-1/CTLA-4 double positive T cells in tumor microenvironment (TME) while reducing systemic toxicity by sparing CTLA-4 single positive cells, making it a potential first-in-class (FIH) or best-in-class (BIC) next-generation immuno-oncology backbone. Preclinical studies have demonstrated that CS2009 induces more potent tumor growth inhibition (TGI) than its potential competitors, such as PD-1/CTLA-4 bispecific antibodies, PD-1/VEGF bispecific antibodies, and PD-1/CTLA-4 combination therapies, along with an outstanding safety profile. CS2009 is currently evaluated in a global multicenter Phase I clinical trial in patients with late-stage cancers, including non-small cell lung cancer (NSCLC), ovarian cancer (OC), renal cell carcinoma (RCC), cervical cancer (CC), hepatocellular carcinoma (HCC), gastric adenocarcinoma (GAC), etc.
CS5006 is a first-in-class ADC targeting the novel antigen ITGB4, whose expression pattern holds broad application potential in solid tumors, including NSCLC, squamous cell carcinoma of the head and neck (SCCHN), and esophageal squamous cell carcinoma (ESCC). Preclinical studies demonstrated that ITGB4 ADCs were potent to inhibit tumor growth in multiple animal models and well tolerated, thus supporting further preclinical development toward clinical evaluation of this promising FIC molecule.
CS2011 (EGFR/HER3 bispecific antibody) is the bispecific antibody backbone of CS5007 (EGFR/HER3 bispecific ADC). CS2011 enables synergistic blocking of EGFR and HER3 signaling for enhanced therapeutic effects, while minimizing toxicity in normal tissues. CS5007 is built on CStone’s proprietary ADC platform, demonstrating best-in-class potential. Both CS2011 and CS5007 target indications include NSCLC, SCCHN, and colorectal cancer (CRC).
CS5005 is a first-in-class ADC targeting SSTR2, enabling precise targeting of SSTR2-positive tumors, including small cell lung cancer (SCLC), neuroendocrine carcinoma (NEC), and neuroendocrine tumors (NETs). CS5005 is composed of CStone’s proprietary anti-SSTR2 antibody with high affinity and selectivity, CStone’s proprietary hydrophilic beta-glucuronide linker, and potent TOP1 inhibitor. It has demonstrated encouraging anti-tumor activity in vitro and in vivo. Meanwhile, leveraging CStone’s proprietary ADC platform, we are accelerating the development of a bispecific ADC targeting SSTR2/DLL3 (CS5008). By simultaneously targeting SSTR2 and DLL3 that frequently co-express in SCLC, NECs, NETs and others, CS5008 aims to overcome tumor heterogeneity, a challenge faced by mono-specific therapies.
Detailed information on the research topics and poster presentations selected for AACR (Free AACR Whitepaper) 2025 are as follows:

Title: CS2009: A first-in-class trispecific antibody targeting PD-1, CTLA-4, and VEGFA with potential to be a next-generation backbone therapy with combined checkpoint inhibition and anti-angiogenesis
Session Title: Overcoming Checkpoint Inhibition and Tumor Suppression
Presentation Type: Poster
Abstract Number: 7299
Time: Wednesday, April 30, 2025, 9:00 AM – 12:00 PM ET
Location: Poster Section 39, Board #14
Key Findings: In the proof of mechanism studies, CS2009 demonstrated strong synergy between the PD-1 and CTLA-4 arms, and the checkpoint inhibitory activity from the PD-1/CTLA4 arms was also greatly enhanced through crosslinking between its anti-VEGF arms with VEGFA dimers. DMPK/toxicology study in cynomolgus monkeys demonstrated that the highest non-severely toxic dose (HNSTD) and the no observed adverse effect level (NOAEL) of CS2009 were 100 mg/kg. CS2009 exhibited a PK profile comparable to those of monoclonal antibodies and demonstrated dose-dependent T-cell activation in cynomolgus monkeys.

Title: CS5006: A novel integrin β4-targeted antibody-drug conjugate (ADC) with robust antitumor activity in preclinical studies
Session Title: Growth Factor Receptors and Other Surface Antigens as Targets for Therapy 2
Presentation Type: Poster
Abstract Number: 2953
Date & Time: Monday, April 28, 2025, 2:00 PM – 5:00 PM ET
Location: Poster Section 18, Board #5
Key Findings: CS5006 (ITGB4 ADC) demonstrated promising therapeutic potential by effectively killing tumor cells in both in vivo and in vitro studies, while maintaining a PK profile comparable to those of monoclonal antibodies.

Title: CS2011: A novel bispecific antibody targeting EGFR and HER3 that demonstrates promising antitumor activity in preclinical evaluation
Session Title: Growth Factor Receptors and Other Surface Antigens as Targets for Therapy 1
Presentation Type: Poster
Abstract Number: 2927
Date and Time: Monday, April 28, 2025, 2:00 PM – 5:00 PM ET
Location: Poster Section 17, Board #1
Key Findings: CS2011 (an EGFR/HER3 bispecific antibody), composed of anti-EGFR and anti-HER3 arms with balanced affinity, effectively and synergistically inhibits EGFR/HER3 downstream signaling, leading to further inhibition of tumor growth. Its lead compound demonstrated favorable stability and a PK profile comparable to those of monoclonal antibodies.

Title: CS5007: A novel EGFR and HER3 dual-targeted antibody-drug conjugate (ADC) with potent antitumor activity in preclinical studies
Session Title: Growth Factor Receptors and Other Surface Antigens as Targets for Therapy 2
Presentation Type: Poster
Abstract Number: 2954
Date and Time: Monday, April 28, 2025, 2:00 PM – 5:00 PM ET
Location: Poster Section 18, Board #6
Key Findings: CS5007 (EGFR/HER3 ADC) inhibited tumor growth by blocking downstream EGFR/HER3 signaling and releasing chemotherapeutic molecules in a target-dependent manner. Its lead compound demonstrated favorable stability and a PK profile comparable to those of monoclonal antibodies.

Title: CS5005: A novel SSTR2-targeted antibody-drug conjugate (ADC) with robust antitumor activity in preclinical studies
Session Title: Molecular, Preclinical, and Clinical Endocrinology
Presentation Type: Poster
Abstract Number: 4751
Date & Time: Tuesday, April 29, 2025, 9:00 AM – 12:00 PM ET
Location: Poster Section 35, Board #18
Key Findings: CS5005 (SSTR2 ADC) demonstrated promising therapeutic potential by effectively killing tumor cells in both in vivo and in vitro studies, while maintaining a PK profile comparable to those of monoclonal antibodies. Additionally, a dual-target ADC against DLL3 and SSTR2 also exhibited potential as a therapeutic agent.

On March 25, 2025 Actinium Pharmaceuticals, Inc. (NYSE AMERICAN: ATNM) (Actinium or the Company), a pioneer in the development of targeted radiotherapies, reported it will host an investor call at 8:00 am ET that will feature KOL Dr. Ehab Atallah, Professor of Medicine at the Medical College of Wisconsin and principal investigator of the Actimab-A + CLAG-M combination trial in patients with relapsed/refractory acute myeloid leukemia (r/r AML) (Press release, Actinium Pharmaceuticals, MAR 25, 2025, View Source [SID1234651422]). Dr. Atallah will discuss Actimab-A clinical results to date including recently published long-term survival outcomes and the planned pivotal Phase 2/3 clinical trial in r/r AML and trials to be conducted under Actinium’s cooperative research and development agreement (CRADA) with the National Cancer Institute (NCI). In addition, Actinium’s management will detail its recently announced Actimab-A solid tumor program, which is comprised of several controlled, head-to-head clinical trials that will evaluate the combination of Actimab-A with KEYTRUDA versus KEYTRUDA alone, and Actimab-A with OPDIVO versus OPDIVO alone initially in patients with head and neck squamous cell carcinoma and non-small cell lung cancer with a separate trial for each indication.

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Actinium’s company update will highlight the 3 separate potential multi-billion-dollar blockbuster market opportunities being pursued with its targeted radiotherapies including the following:

– Actimab-A as a mutation agnostic, backbone therapy for myeloid malignancies including AML and myelodysplastic syndromes (MDS) across multiple treatment settings

– Actimab-A as a pan solid tumor therapy in combination with PD-1 inhibitors including KEYTRUDA and OPDIVO by depleting myeloid derived suppressor cells (MDSCs)

– Iomab-ACT as a universal targeted conditioning agent to increase patients access to cell & gene therapies and improve patient outcomes

To register for the KOL Call & Company Update please use the following link:

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On March 25, 2025 Oncotelic Therapeutics, Inc (OTCQB:OTLC) ("Oncotelic", the "Company" or "We" or "Our"), "), a leader in RNA-based therapeutics, reported the successful completion of a Phase 1 clinical trial evaluating OT-101, in combination with IL-2 for advanced or metastatic solid tumors (Press release, Oncotelic, MAR 25, 2025, View Source [SID1234651421]). These results set the stage for new studies that combine OT-101,an antisense therapeutic targeting Transforming Growth Factor Beta 2 (TGFβ2), with checkpoint inhibitors ("CKIs") and recombinant IL-2 (aldesleukin) ("IL-2").

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The announcement coincides with a presentation delivered by Vuong Trieu, Ph.D., Chairman & CEO of Oncotelic, at the 5th Symposium on World Cancer Research (SWCR) 2025. In his talk, titled "Transforming Growth Factor Beta 2 in Aging, Cancer, Lupus, and Immuno-Oncology: A Convergence of Disease Pathways and Therapeutic Potential," Dr. Trieu described the central role of TGFβ2 in immune suppression across multiple diseases, and outlined the ongoing development of OT-101 in pancreatic cancer (Phase 3 STOP-PC study), gliomas, and combination regimens with immunotherapies.

Phase 1 Trial of OT-101 (TASO) and IL-2 Successfully Completed

The Phase 1 trial (ClinicalTrials.gov ID: NCT04862767) investigated the safety and tolerability of OT-101 in combination with recombinant IL-2 in patients with advanced or metastatic solid tumors.
The combination showed a tolerable safety profile at the planned dosing schedule, with no unexpected safety signals identified.
Based on the favorable safety data, Oncotelic plans to advance OT-101 plus IL-2 into further clinical studies, exploring synergies with CKIs such as PD-1 blockers.
Key Highlights From the Kyoto 2025 Presentation

TGFβ2’s Central Role in Cancer and Beyond:
Dr. Trieu presented evidence that TGFβ2 is a critical driver of immunosuppression, fueling tumor progression by promoting an M2-like macrophage phenotype and blunting antitumor immunity.
OT-101’s Clinical Progress and Versatility:
In pancreatic ductal adenocarcinoma (PDAC), OT-101 is currently in a Phase 3 clinical trial (the STOP-PC study) combined with mFOLFIRINOX.
OT-101 has shown encouraging activity in gliomas, where high intratumoral TGFβ2 expression correlates with poor prognosis.
Combination regimens with CKIs and IL-2 address multiple pathways of immune evasion, potentially amplifying therapeutic benefits.
Next Studies Targeting TGF β2 and Beyond:
With the newly completed OT-101 and IL-2 Phase 1 trial, Oncotelic is poised to begin further combination trials to determine the added efficacy of OT-101, IL-2, and CKIs in solid tumors such as lung cancer, melanoma, and colorectal cancer.
Next wave of clinical trials aiming to knock down TGF β 2 (e.g., with OT-101) paired with intervention with a complementary therapy, checkpoint blockade, IL-2, interferon-based regimens, or standard-of-care chemo, depending on the tumor indication
"We are thrilled to announce the completion of our Phase 1 study evaluating OT-101 with IL-2, a key milestone that sets the stage for next-generation immunotherapy combinations," said Dr. Vuong Trieu, Chairman & CEO of Oncotelic. Our findings reinforce that OT-101’s specific inhibition of TGFβ2 can significantly enhance the immune response, and we are eager to test these synergies with checkpoint inhibitors and IL-2 to maximize therapeutic potential for patients with hard-to-treat cancers."

The presentation, along with a chatbot powered by PDAOAI, can be accessed on our new PDAOAI public Discord: View Source

Our PDAOAI Discord server allows members of the public to view and download the presentation. In addition, by using "/query", they can utilize our proprietary chatbot technology to ask questions related to the presentation. We highly recommend joining Discord. If you need any help, members of the PDAOAI team can assist. In addition, you can use "/help". We intend to use this server for our PDAOAI platform. For those who are interested in joining our investor Discord, can do so here: View Source

"We are excited to bring PDAOAI to the public and are excited for the user feedback. This presentation is a beginning to bringing our AI technology to the masses and not just our internal team," said Scott Myers, Product Manager.

On March 25, 2025 Molecular Partners AG (SIX: MOLN; NASDAQ: MOLN), a clinical-stage biotech company developing a new class of custom-built protein drugs known as DARPin therapeutics ("Molecular Partners" or the "Company"), reported it will hold three poster presentations at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2025, taking place April 25-30 in Chicago, IL (Press release, Molecular Partners, MAR 25, 2025, View Source [SID1234651420]).

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Details of the presentations:

MP0712, the first anti-DLL3 212Pb Radio-DARPin (RDT) candidate for targeted radiotherapy of small cell lung cancer (SCLC)
Session Category: Experimental and Molecular Therapeutics
Session Title: Biochemical Modulators of Cancer / Differentiation Therapeutic Strategies
Session Timing: Sunday April 27 at 2:00pm – 5:00pm CST
Location: Poster Section 16, Poster Board Number: 13
Published Abstract Number: 346

Development of 212Pb-based Radio-DARPin therapy (RDT) for the treatment of mesothelin (MSLN)-positive solid tumors
Session Category: Experimental and Molecular Therapeutics
Session Title: Biochemical Modulators of Cancer / Differentiation Therapeutic Strategies
Session Timing: Sunday April 27 at 2:00 – 5:00pm CST
Location: Poster Section 16, Poster Board Number: 6
Published Abstract Number: 339

Next-generation multi-specific and conditionally activated CD3 Switch-DARPins with CD2 co-stimulation to tackle the current limitations of T cell engagers in solid tumors
Session Category: Experimental and Molecular Therapeutics
Session Title: Therapeutic Approaches to Attack the Tumor Microenvironment
Session Timing: Monday April 28 at 2:00pm – 5:00pm CST
Location: Poster Section 24, Poster Board Number: 3
Published Abstract Number: 3119

On March 25, 2025 Verastem Oncology (Nasdaq: VSTM), a biopharmaceutical company committed to advancing new medicines for patients with RAS/MAPK pathway-driven cancers, reported multiple oral and poster presentations at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2025 to be held on April 25-30 in Chicago, Illinois (Press release, Verastem, MAR 25, 2025, View Source [SID1234651419]). These presentations will highlight clinical and preclinical data from the Company’s development programs, including VS-7375 (GFH375), an oral KRAS G12D (ON/OFF) inhibitor and avutometinib, an oral RAF/MEK clamp, and defactinib, an oral FAK inhibitor.

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"At this year’s AACR (Free AACR Whitepaper) annual meeting, we show that VS-7375, our oral KRAS G12D (ON/OFF) inhibitor, was found to be more potent than other KRAS G12D inhibitors in preclinical models. In addition, using a patient-derived LGSOC xenograft model, we and our collaborators further explored the mechanism by which our FAK inhibitor increases the anti-tumor efficacy of avutometinib. The results demonstrate that compared to avutometinib alone, the FAK inhibitor/avutometinib combination inhibits RAS/MAPK pathway signaling more deeply while also blocking key adaptive resistance mechanisms including PI3K and YAP/TEAD signaling," said Jonathan Pachter, Ph.D., Chief Scientific Officer of Verastem Oncology.

Key Data Presentations:

Oral Presentation: Minisymposium

Title: Correlative preclinical studies to elucidate mechanisms of synergy of the combination of the RAF/MEK clamp avutometinib and the FAK inhibitor defactinib in low-grade serous ovarian cancer
Abstract #: 6368
Presenter: Udai Banerji, M.D.
Session: Targeted Therapies and Combinations, Clinical Research
Session Date/Time: April 29, 2025 from 2:30 to 4:30 pm CST
In a patient-derived LGSOC xenograft model, addition of a FAK inhibitor with avutometinib augmented tumor regression, more strongly inhibited RAS/MAPK pathway signaling compared to avutometinib alone and suppressed multiple putative mechanisms of resistance to avutometinib monotherapy including PI3K and YAP/TEAD signaling.

Poster Presentations:

Title: GFH375 (VS-7375): An oral, selective KRAS G12D (ON/OFF) inhibitor with potent anti-tumor efficacy as single agent and in combination with other anticancer therapies in preclinical models
Abstract #: 4394
Session: ​RAS Inhibitors, Experimental and Molecular Therapeutics
Location/Poster Board #: Poster Section 21, Board # 29
Date and Time: April 29, 2025 from 9:00 am to 12:00 pm CST
VS-7375 (GFH375), a selective oral KRAS G12D (ON/OFF) inhibitor, was found to be more potent than other KRAS G12D inhibitors in preclinical models. In addition, the combination of VS-7375 with the anti-EGFR antibody, cetuximab, induced strong tumor regressions in preclinical models, including complete responses in all mice in a colorectal cancer model.

Title: RAF/MEK clamp avutometinib combined with a pan-RAF inhibitor induces nearly complete MAPK pathway inhibition with deep tumor regressions in NRAS or BRAF class III mutant models
Abstract #: 4393
Session: ​RAS Inhibitors, Experimental and Molecular Therapeutics
Location/Poster Board #: Poster Section 21, Board # 28
Date and Time: April 29, 2025 from 9:00 am to 12:00 pm CST
Combining avutometinib with a pan-RAF inhibitor (exarafenib or belvarafenib) led to strong tumor regressions in multiple NRAS- and BRAF-driven tumor models corresponding with nearly complete inhibition of RAS/MAPK pathway signaling.

Late-Breaking and Clinical Abstracts:

Title: A Single-Arm Phase 1 Trial of Avutometinib (RAF/MEK inhibitor), Abemaciclib (Abema), and Fulvestrant in CDK4/6 inhibitor (CDK4/6i)-pretreated patients (pts) with HR+ Metastatic Breast Cancer (MBC) – Investigator-Sponsored Trial
Abstract #: CT028
Session: Phase 0 and Phase I Clinical Trials
Location/Poster Board #: Poster Section 49, Board #7
Date and Time: April 28, 2025 from 9:00 am to 12:00 pm CST
Title: Mechanistic rationale for combination of RAF/MEK glue avutometinib with a pan-RAF inhibitor for RAS-mutant tumor-selective therapy
Abstract #: LB424
Session: ​ Late-Breaking Research: Experimental and Molecular Therapeutics 4
Location/Poster Board #: Poster Section 51, Board #6
Date and Time: April 30, 2025 from 9:00 am to 12:00 pm CST
The accepted abstracts are available on the AACR (Free AACR Whitepaper) conference website: AACR (Free AACR Whitepaper) Annual Meeting 2025 | Meetings | AACR (Free AACR Whitepaper). Late-breaking and clinical abstracts will be available on April 25, 2025.

About the Avutometinib and Defactinib ​​Combination

Avutometinib is an oral RAF/MEK clamp that potently inhibits MEK1/2 kinase activities and induces inactive complexes of MEK with ARAF, BRAF, and CRAF, potentially creating a more complete and durable anti-tumor response through maximal RAS/MAPK pathway inhibition. In contrast to currently available MEK-only inhibitors, avutometinib blocks both MEK kinase activity and the ability of RAF to phosphorylate MEK. This unique mechanism allows avutometinib to block MEK signaling without the compensatory activation of MEK that appears to limit the efficacy of the MEK-only inhibitors.

Defactinib is an oral, selective inhibitor of focal adhesion kinase (FAK) and proline-rich tyrosine kinase-2 (Pyk2), the two members of the focal adhesion kinase family of non-receptor protein tyrosine kinases. FAK and Pyk2 integrate signals from integrin and growth factor receptors to regulate cell proliferation, survival, migration, and invasion. FAK activation has been shown to mediate resistance to multiple anti-cancer agents, including RAF and MEK inhibitors.

Verastem Oncology is currently conducting clinical trials with avutometinib with and without defactinib in RAS/MAPK-driven tumors as part of its Raf And Mek Program or RAMP. Verastem is currently enrolling patients and activating sites for RAMP 301 (GOG-3097/ENGOT-ov81/NCRI) (NCT06072781), an international Phase 3 confirmatory trial evaluating the combination of avutometinib and defactinib versus standard chemotherapy or hormonal therapy for the treatment of recurrent low-grade serous ovarian cancer (LGSOC).

Verastem was granted Priority Review and a Prescription Drug User Fee Act (PDUFA) date of June 30, 2025, for its New Drug Application (NDA) to the U.S. Food and Drug Administration (FDA), for the investigational combination of avutometinib and defactinib in adults with recurrent KRAS mutant LGSOC who received at least one prior systemic therapy. Verastem initiated a rolling NDA in May 2024 to the FDA and completed its NDA submission in October 2024. The FDA granted Breakthrough Therapy Designation for the treatment of patients with recurrent LGSOC after one or more prior lines of therapy, including platinum-based chemotherapy, in May 2021. Avutometinib alone or in combination with defactinib was also granted Orphan Drug Designation by the FDA for the treatment of LGSOC.

Verastem Oncology has established a clinical collaboration with Amgen to evaluate LUMAKRAS (sotorasib) in combination with avutometinib and defactinib in both treatment-naïve patients and in patients whose KRAS G12C mutant non-small cell lung cancer progressed on a G12C inhibitor as part of the RAMP 203 trial (NCT05074810). Verastem has received Fast Track Designation from the FDA for the triplet combination in April 2024. RAMP 205 (NCT05669482), a Phase 1b/2 clinical trial evaluating avutometinib and defactinib with gemcitabine/nab-paclitaxel in patients with front-line metastatic pancreatic cancer, is supported by the PanCAN Therapeutic Accelerator Award. FDA granted Orphan Drug Designation to the avutometinib and defactinib combination for the treatment of pancreatic cancer.

About VS-7375, an Oral KRAS G12D (ON/OFF) Inhibitor

VS-7375 is a potential best-in-class, potent, and selective oral KRAS G12D dual ON/OFF inhibitor. VS-7375 is the lead program from the Verastem Oncology discovery and development collaboration with GenFleet Therapeutics. Verastem filed an investigational new drug (IND) application in the U.S. for VS-7375 in the first quarter of 2025. GenFleet’s IND for VS-7375 (known as GFH375 in China) was approved in China in June 2024, and the first patient was dosed in a Phase 1/2 study in July 2024.