Biologically Active Small Molecules

Aspirin-d₄ is intended for use as an internal standard for the quantification of aspirin (Item No. 70260) by GC- or LC-MS.

An inhibitor of RET (IC₅₀ = 0.88 &microM), FLT3 (Ki = 0.12 &microM), KDR, c-Abl, and c-Kit demonstrates antiproliferative activity in various cancer cells, including those with RET or FLT3 mutations.

An inhibitor of RET (IC₅₀ = 0.88 &microM), FLT3 (Ki = 0.12 &microM), KDR, c-Abl, and c-Kit demonstrates antiproliferative activity in various cancer cells, including those with RET or FLT3 mutations.

An inhibitor of RET (IC₅₀ = 0.88 &microM), FLT3 (Ki = 0.12 &microM), KDR, c-Abl, and c-Kit demonstrates antiproliferative activity in various cancer cells, including those with RET or FLT3 mutations.

An inhibitor of RET (IC₅₀ = 0.88 &microM), FLT3 (Ki = 0.12 &microM), KDR, c-Abl, and c-Kit demonstrates antiproliferative activity in various cancer cells, including those with RET or FLT3 mutations.

Astaxanthin is a carotenoid pigment found primarily in marine animals including shrimp and salmon it is a potent lipid-soluble antioxidant.

Astaxanthin is a carotenoid pigment found primarily in marine animals including shrimp and salmon it is a potent lipid-soluble antioxidant.

A histamine H1 receptor antagonist (Ki = 4.4 nM) that also blocks ERG potassium channels (IC₅₀ = ~1 nM) used to study long QT syndrome type 2 and as an antineoplastic agent for decreasing proliferation of various cancer cells.

A histamine H1 receptor antagonist (Ki = 4.4 nM) that also blocks ERG potassium channels (IC₅₀ = ~1 nM) used to study long QT syndrome type 2 and as an antineoplastic agent for decreasing proliferation of various cancer cells.

A histamine H1 receptor antagonist (Ki = 4.4 nM) that also blocks ERG potassium channels (IC₅₀ = ~1 nM) used to study long QT syndrome type 2 and as an antineoplastic agent for decreasing proliferation of various cancer cells.

An antibiotic fungal metabolite that completely inhibits the binding of the potent vasoconstrictor ET-1 to the ETA receptor in A10 cells at 0.1 &muM also inhibits VEGF-induced tube formation of HUVECs at 3-10 &muM.

An antibiotic fungal metabolite that completely inhibits the binding of the potent vasoconstrictor ET-1 to the ETA receptor in A10 cells at 0.1 &muM also inhibits VEGF-induced tube formation of HUVECs at 3-10 &muM.