HDAC-IN-56 

HDAC-IN-56 ((S)-17b) is an orally active class I histone deacetylase (HDAC) inhibitor with IC₅₀ values of 56.0 ± 6.0, 90.0 ± 5.9, 422.2 ± 105.1, >10000 nM for HDAC1, HDAC2, HDAC3, and HDAC4-11, respectively. HDAC-IN-56 has potent inhibitory activity while strongly increasing intracellular levels of acetylhistone H3 and P21 and effectively inducing G1 cell cycle arrest and apoptosis.HDAC-IN-56 has antitumor activity ^[1].

HDAC-IN-56 shows potent and selective inhibition against Class I HDACs 1, 2, and 3, better than that of MS-275 (HY-12163)^[1].
HDAC-IN-56 (0.1 μM, 2 h) is metabolized in human, monkey, dog, rat and mouse hepatocytes with significant species differences and was stable in five species of hepatocytes^[1].
HDAC-IN-56 (0.01-1 μM, 72 h) effectively induces G1 cell cycle arrest and apoptosis^[1].
HDAC-IN-56 (0.01-1 μM, 72 h) treatment increases the intracellular level of acetyl-histone H3 and p21 simultaneously better than that of Tucidinostat (HY-109015) or MS-275 (HY-12163), which implied its strong class I histone deacetylase inhibition^[1].
HDAC-IN-56 has an IC₅₀ of 139.0 ± 8.0 nM for SKM-1^[1].
HDAC-IN-56 shows potent and selective inhibition against Class I HDACs 1, 2, and 3, better than that of MS-275 (HY-12163)^[1].
HDAC-IN-56 (0.1 μM, 2 h) is metabolized in human, monkey, dog, rat and mouse hepatocytes with significant species differences and was stable in five species of hepatocytes^[1].
HDAC-IN-56 (0.01-1 μM, 72 h) effectively induces G1 cell cycle arrest and apoptosis^[1].
HDAC-IN-56 (0.01-1 μM, 72 h) treatment increases the intracellular level of acetyl-histone H3 and p21 simultaneously better than that of Tucidinostat (HY-109015) or MS-275 (HY-12163), which implied its strong class I histone deacetylase inhibition^[1].
HDAC-IN-56 has an IC₅₀ of 139.0 ± 8.0 nM for SKM-1^[1].
HDAC-IN-56 (compuond (S)-17b) Metabolic Stability in Hepatocytes of Five Species (mass spectrum peak area)^[1]

HDAC-IN-56 (compuond (S)-17b) 五个物种的肝细胞中的代谢稳定性 (质谱峰面积)^[1]

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

HDAC-IN-56 (10-80 mg/kg/d, p.o., one month) cause no significant change of body weight, even at high dose of 80 mg/kg per day, the mice can tolerate with the descended body weight compared with the control^[1].
HDAC-IN-56 (SD: 10, 20 mg/kg ; ICR: 20, 40 mg/kg, p.o.) represent a favorable pharmacokinetic profile with an oral bioavailability of 47.7% in ICR mice and 39.5% in SD rat, respectively^[1].
HDAC-IN-56 (20-60 mg/kg, p.o.) inhibit the tumor growth of MC38 cells in nude mice as expected, when inoculate in immunocompetent C57BL/6 mice show more significant tumor growth inhibition at the same doses, which implie that the immune system may be engaged and somehow activated gain stronger antitumor effect^[1].
In vivo pharmacokinetics of HDAC-IN-56 (compuond (S)-17b) in ICR mice and SD rat^[1]

HDAC-IN-56（compuond (S)-17b）在ICR小鼠和SD大鼠体内的药代动力学研究^[1]

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

485.55

C₂₈H₂₈FN₅O₂

2814571-89-4

O=C1C=CC(C2=CC=C(C=C2)CN(C)C)=NN1[C@H](C3=CC=C(C=C3)C(NC4=C(N)C=C(C=C4)F)=O)C

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Li D, et al. Discovery of (S)-N-(2-Amino-4-fluorophenyl)-4-(1-(3-(4-((dimethylamino)methyl)phenyl)-6-oxopyridazin-1(6H)-yl)ethyl) benzamide as Potent Class I Selective HDAC Inhibitor for Oral Anticancer Drug Candidate. J Med Chem. 2023 May 25;66(10):7016-7037.  [Content Brief]