Date published: 2025-10-25

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TDAG8 Inhibitors

TDAG8 Inhibitors constitute a distinctive and specialized chemical class designed to interact with the TDAG8 receptor, also recognized as GPR65, a member of the G protein-coupled receptor family. This receptor is notably expressed on the cell surfaces of immune cells, with a predominant presence in specific subsets of T cells and dendritic cells. TDAG8 receptor, localized mainly in immune tissues and organs, serves as a pivotal mediator in the regulation of intracellular pH levels within immune cells. The inhibitors developed for TDAG8 demonstrate a unique chemical fingerprint tailored to bind with this receptor in a highly selective manner. This molecular interaction holds the potential to modulate the downstream signaling cascades and cellular responses associated with immune functions. Characterized by a distinct structural composition, TDAG8 inhibitors are carefully crafted compounds that are adept at obstructing the activation of the TDAG8 receptor.

By doing so, they may influence a spectrum of cellular processes that hinge on pH homeostasis and intracellular pH dynamics. Importantly, these inhibitors are designed with precision to minimize unintended interference with the essential pH-regulating functions of TDAG8, focusing instead on its potential to modulate immune responses. The chemical architecture of TDAG8 inhibitors, devised through meticulous design and optimization, allows for the establishment of a reversible bond with the TDAG8 receptor. This bond can potentially lead to alterations in the conformation and activity of the receptor, subsequently impacting the associated signaling pathways and cellular behaviors. Such targeted interactions could open avenues for innovative research aimed at comprehending the intricate role of the TDAG8 receptor in immune regulation. The development and study of TDAG8 inhibitors contribute to the broader understanding of immune responses and hold promise for uncovering novel insights into immune cell behavior modulation.

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