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BioWorld - Tuesday, March 3, 2026
Home » Topics » AACR-NCI-EORTC Molecular Targets and Cancer Therapeutics, BioWorld Science

AACR-NCI-EORTC Molecular Targets and Cancer Therapeutics, BioWorld Science
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3D illustration demonstrating antibody-drug conjugate.
Immuno-oncology

IKS-012, a novel and potent ADC, for the treatment of FRα-positive cancers

Nov. 6, 2024
Iksuda Therapeutics Ltd. disclosed the design of a novel, effective and safe antibody-drug conjugate (ADC), IKS-012, for the potential treatment of folate receptor α (FRα)-positive cancers.
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Cancer

AVA-6103 for the treatment of FAP-positive cancer by targeting topoisomerase

Nov. 6, 2024
Avacta Life Sciences (Avacta Group plc) presented preclinical data on AVA-6103, a second-generation Precision peptide-drug conjugate, being developed for the potential treatment of cancer. AVA-6103 was developed using the company’s proprietary Precision technology incorporating a dipeptide specifically cleaved by fibroblast activation protein α (FAPα) leading to tumor-specific delivery of exatecan directly into the tumor cells.
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Pill over molecule structures
Cancer

VRTX-531 demonstrates best-in-class USP1 inhibitor activity in preclinical models

Nov. 5, 2024
Researchers from Vrise Therapeutics Inc. and Vegen Therapeutics Pvt Ltd. presented preclinical data for VRTX-531, an allosteric inhibitor of ubiquitin carboxyl-terminal hydrolase 1 (USP1), being developed for the treatment of cancer.
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Cancer cells under magnifying glass
Cancer

ADT-1004, a promising pan-RAS inhibitor, shows efficacy in PDAC

Nov. 5, 2024
Pancreatic ductal adenocarcinoma (PDAC) has a low 5-year survival rate of <12%. Even though KRAS is mutated in about 88% of PDACs, the KRAS G12C mutation is rare, limiting the use of KRAS G12C inhibitors. Hence, there is a need for pan-RAS inhibitors to cover the broad RAS mutation spectrum in PDAC.
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Cancer cell targeted in crosshairs
Cancer

Remix’s REM-422 induces potent antitumor activity in preclinical adenoid cystic carcinoma

Nov. 4, 2024
The c-MYB oncogene plays a key role in hematopoietic cell differentiation and proliferation. Genetic abnormalities and dysregulation of MYB have been found in several cancers, including adenoid cystic carcinoma (ACC) (80% of cases), making it an attractive druggable target for ACC treatment.
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Drug R&D concept image.
Cancer

Next-generation PARP1 inhibitor shows high synergistic scores

Nov. 4, 2024
PARP1 is critical for repairing DNA single-strand breaks. First-generation PARP1/2 inhibitors have proven effective in the treatment of tumors with mutations in the essential homologous recombination repair (HR) genes including BRCA mutations. However, hematological toxicity associated with PARP2 emphasizes the need to find second-generation compounds with better safety profiles.
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Cancer

ABSK-141 exhibits strong anti-KRAS G12D activity

Nov. 4, 2024
Researchers from Abbisko Therapeutics Inc. presented the preclinical characterization of ABSK-141, a potent bioavailable small-molecule KRAS G12D inhibitor.
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Illustration of tumor
Cancer

AZD-3470 displays robust PK/PD/efficacy relationship, antitumor activity

Nov. 4, 2024
Researchers from Astrazeneca plc recently reported preclinical data for AZD-3470, a second-generation MTA-cooperative PRMT5 inhibitor currently in early clinical development for the treatment of patients with MTAP-deficient solid tumors (NCT06130553) and hematological cancers (NCT06137144).
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Illustration of dividing cancer cells
Cancer

MC-339 exerts antitumor activity in DLL3-positive tumors

Oct. 31, 2024

Researchers from Mariana Oncology Inc. reported preclinical data on MC-339, a DLL3-targeting macrocyclic peptide in several tumor models. Delta-like ligand 3 (DLL3) is overexpressed on the cell surface of small-cell lung cancer (SCLC), neuroendocrine prostate cancer (NEPC) and metastatic melanoma.


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Illustration of chronic lymphocytic leukemia cells
Cancer

CFON-026 inhibits clinically relevant BTK inhibitor mutations

Oct. 31, 2024
Bruton tyrosine kinase (BTK) inhibitors are commonly used in the treatment of hematological cancers. However, approximately 67% of patients with relapsed chronic lymphocytic leukemia (CLL) develop resistance to acalabrutinib and ibrutinib due to mutations in BTK, initially most often C481S.
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