Seed Therapeutics Inc.’s ST-01156 has been awarded orphan drug designation for the treatment of Ewing sarcoma as well as rare pediatric disease designation by the FDA.
Son of sevenless homolog 1 (SOS1) is an essential guanine nucleotide exchange factor (GEF) in KRAS-driven tumors, and it also functions as a downstream node protein of BCR-ABL, suggesting its critical role in the pathogenesis of chronic myeloid leukemia (CML). Investigators at Shanghaitech University have reported the discovery and preclinical characterization of a novel potent SOS1 proteolysis targeting chimera (PROTAC) – SIAIS-562055 – being developed as an anticancer agent.
In the preclinical setting, inhibitors of histone deacetylase 6 (HDAC6) have proven effective at reducing liver inflammation through modulation of the immune response.
Immune checkpoint blockade is one of the major advances in cancer treatment in recent years. However, the majority of immune checkpoints are embedded in the cell membrane and this fact represents a limitation for targeted degradation using proteolysis-targeting chimeras (PROTACs).
Aromatase inhibitors (AI) are among the most widely used therapies in the treatment of breast tumors expressing estrogen receptor α (ERα). Alone or in combination with other agents, they are the standard of care for hormone receptor-positive tumors.
The protease mucosa-associated lymphoid tissue lymphoma translocation 1 (MALT1) is a signaling protein with both molecular scaffolding and protease activity involved in lymphocyte activation. MALT1 is considered a therapeutic target for chronic lymphocytic leukemia (CLL) in patients who develop resistance to Bruton tyrosine kinase (BTK) inhibitors.
Researchers from AUTOTAC Bio Inc. and affiliated organizations presented preclinical data for ATC-324, a novel autophagy-targeting chimera (AUTOTAC) designed to induce androgen receptor (AR) degradation.
MBT-C101 is a selective, potentially first-in-class potent HSP90 chaperone-mediated degrader of PI3Kα, for the treatment of breast cancer. It was developed by Magicbullet Therapeutics Inc. using the company’s Chaperone-mediated Degrader (CM-Degrader) platform.
The transcription factor IKZF2 is a marker of highly suppressive regulatory T cells (Tregs). When IKZF2 is degraded, Tregs become effector-like T cells leading to increased antitumor immune response in the tumor microenvironment.
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