ruxolitinib

Ruxolitinib (INCB018424) is a JAK1 2 inhibitor (IC50=3.3 2.8 nM) that is potent and selective. Rixolitinib exhibits antitumor activity and induces autophagy and apoptosis.

Ruxolitinib phosphate (INCB18424 phosphate) is a JAK1 2 inhibitor with IC50 of 3.3 nM 2.8 nM. Its selectivity for JAK1 2 is more than 130 times that of JAK3.

Ruxolitinib S enantiomer (INCB18424) is the S-enantiomer of Ruxolitinib. Ruxolitinib is the first potent, selective JAK1 2 inhibitor.

S-Ruxolitinib can be used in related research in the field of life sciences. Its product number is T3066 and CAS number is 1160597-27-2.

Ruxolitinib sulfate (INCB018424 sulfate) is a potent, selective inhibitor of JAK1 2 with IC50 values of 3.3 nM 2.8 nM, demonstrating over 130-fold selectivity for JAK1 2 compared to JAK3.

Deuruxolitinib functions as an inhibitor of JAK1 2.

INCB032304 is an important pharmaceutical intermediate. It can be used in the preparation of Ruxolitinib phosphate (I008849), a janus kinase inhibitor, and in the preparation of Barretinib.

StA-IFN-1 is an inhibitor of the interferon (IFN) induction pathway with an IC50 value of 4.1 μM in a GFP reporter assay for IFN induction similar to TPCA-1 , which specifically inhibits the IKKβ component of the IFN induction pathway. It does not show inhibitory activity in a GFP reporter assay for IFN signaling in which ruxolitinib , which is specific for the IFN signaling component JAK1, is active. StA-IFN-1 reduces the levels of IFN-β, but not ISG MxA, mRNA, suggesting that it is selective for the IFN induction pathway and not the IFN signaling pathway.

SJ988497 is a PROTAC JAK2 degrader that effectively inhibits proliferation in CRLF2-rearranged (CRLF2r) cells and facilitates the degradation of the CRBN neosubstrate GSPT1. Composed of a Ruxolitinib derivative, a linker, and the CRBN ligand Pomalidomide, SJ988497 is utilized in researching acute lymphoblastic leukemia (ALL) [1].

PPL agonist-1 (Compound I-3) is a highly selective agonist of Periplakin (PPL) that raises cAMP levels by modulating PPL, enhancing MITF expression, and consequently promoting melanin synthesis. Additionally, it stimulates melanin production by regulating tryptophan metabolism. Compared to Ruxolitinib, PPL agonist-1 demonstrates superior effectiveness and holds potential for vitiligo research.