set-2

SET 2 is an antagonist of transient receptor potential vanilloid type 2(TRPV2) with an IC50 of 0.46 μM. SET 2 shows selectivity over TRPV1, TRPV3 and TRPV4.

NMS-P953 is a JAK2 inhibitor, displaying significant tumor growth inhibition in SET-2 xenograft tumor model. NMS-P953 has a mechanism of action confirmed in vivo by typical modulation of known biomarkers, and with a favorable pharmacokinetic and safety profile.

MS159 is a potent PROTAC degrader targeting the nuclear receptor binding SET structural domain protein 2 (NSD2), which inhibits tumor cell growth. This compound serves as a valuable chemical tool for investigating NSD2's function in health and disease [1].

NSD2-IN-1 (compound 38) serves as a potent and highly selective inhibitor of NSD2-PWWP1 (nuclear receptor-binding SET domain 2-PWWP1), demonstrating an IC50 value of 0.11 μM. By binding to NSD2-PWWP1, NSD2-IN-1 impacts the expression of genes under NSD2 regulation, leading to apoptosis and cell cycle arrest [1].

DC 432, a potent peptidomimetic inhibitor of N-terminal methyltransferase 1/2 (NTMT1/2) with an IC50 value of 54 nM, incorporates a BM30 peptide enhanced by five arginine residues. It effectively reduces the N-terminal methylation level of the regulator of chromosome condensation 1 and SET proteins in HCT116 cells, demonstrating cell permeability.

PFI-2 is an effective, specific and cell-active lysine methyltransferase SETD7 inhibitor (Ki/IC50: 0.33/2 nM), 1000-fold selectivity over other methyltransferases and other non-epigenetic targets.

PFI-2 hydrochloride ((R)-PFI-2 hydrochloride) is a potent, highly selective, and cell-active inhibitor of the methyltransferase activity of SETD7 (IC50: 2 nM), 500 fold active than (S)-PFI-2.

JAK2-IN-7, a selective inhibitor targeting Janus Kinase 2 (JAK2), exhibits inhibitory concentrations (IC50) of 3 nM for JAK2, 11.7 nM for SET-2 cells, and 41 nM for Ba F3 V617F cells, indicative of its potency and selectivity. This compound demonstrates more than 14-fold selectivity against JAK1, JAK3, and FLT3, underlining its specificity. JAK2-IN-7 effectively induces cell cycle arrest at the G0 G1 phase and promotes apoptosis in tumor cells, manifesting significant antitumor activities [1].