GNF362 is a highly selective and potent orally available inhibitor of inositol trisphosphate 3’ kinase B (Itpkb) with an IC50 of 9 nM, it also inhibits Itpka and Itpkc with IC50 values of 20 nM and 19 nM, respectively. It can be used in research to study treatment for T cell-mediated autoimmune diseases.

GNF362 is a highly selective and potent orally available inhibitor of inositol trisphosphate 3’ kinase B (Itpkb) with an IC50 of 9 nM, it also inhibits Itpka and Itpkc with IC50 values of 20 nM and 19 nM, respectively. It can be used in research to study treatment for T cell-mediated autoimmune diseases.

2-APQC is a potent activator of SIRT3 with a Kd value of 2.756 μM. It alleviates myocardial hypertrophy and fibrosis by regulating mitochondrial homeostasis, exhibiting promising cardioprotective potential in vitro and in vivo. It may serve as a potential candidate for future heart failure (HF) therapeutics.

GNF362 is a highly selective and potent orally available inhibitor of inositol trisphosphate 3’ kinase B (Itpkb) with an IC50 of 9 nM, it also inhibits Itpka and Itpkc with IC50 values of 20 nM and 19 nM, respectively. It can be used in research to study treatment for T cell-mediated autoimmune diseases.

2-APQC is a potent activator of SIRT3 with a Kd value of 2.756 μM. It alleviates myocardial hypertrophy and fibrosis by regulating mitochondrial homeostasis, exhibiting promising cardioprotective potential in vitro and in vivo. It may serve as a potential candidate for future heart failure (HF) therapeutics.

2-APQC is a potent activator of SIRT3 with a Kd value of 2.756 μM. It alleviates myocardial hypertrophy and fibrosis by regulating mitochondrial homeostasis, exhibiting promising cardioprotective potential in vitro and in vivo. It may serve as a potential candidate for future heart failure (HF) therapeutics.

2-APQC is a potent activator of SIRT3 with a Kd value of 2.756 μM. It alleviates myocardial hypertrophy and fibrosis by regulating mitochondrial homeostasis, exhibiting promising cardioprotective potential in vitro and in vivo. It may serve as a potential candidate for future heart failure (HF) therapeutics.

Sunvozertinib (DZD9008) is an oral, potent, and selective inhibitor of ErbBs (EGFR or Her2), particularly mutant forms of ErbBs. It also inhibits EGFR exon 20 NPH insertion, EGFR exon 20 ASV insertion, EGFR L858R and T790M mutations, Her2 exon 20 YVMA, and EGFR WT A431, with IC50 values of 20.4 nM, 20.4 nM, 1.1 nM, […]

Sunvozertinib (DZD9008) is an oral, potent, and selective inhibitor of ErbBs (EGFR or Her2), particularly mutant forms of ErbBs. It also inhibits EGFR exon 20 NPH insertion, EGFR exon 20 ASV insertion, EGFR L858R and T790M mutations, Her2 exon 20 YVMA, and EGFR WT A431, with IC50 values of 20.4 nM, 20.4 nM, 1.1 nM, […]

Sunvozertinib (DZD9008) is an oral, potent, and selective inhibitor of ErbBs (EGFR or Her2), particularly mutant forms of ErbBs. It also inhibits EGFR exon 20 NPH insertion, EGFR exon 20 ASV insertion, EGFR L858R and T790M mutations, Her2 exon 20 YVMA, and EGFR WT A431, with IC50 values of 20.4 nM, 20.4 nM, 1.1 nM, […]