| Identification | Back Directory | [Name]
1H-Indole-2-carboxylic acid, 4,6-bis(1-methylethoxy)-, methyl ester | [CAS]
2607143-50-8 | [Synonyms]
1H-Indole-2-carboxylic acid, 4,6-bis(1-methylethoxy)-, methyl ester | [Molecular Formula]
C16H21NO4 | [MOL File]
2607143-50-8.mol | [Molecular Weight]
291.34 |
| Chemical Properties | Back Directory | [Boiling point ]
439.9±40.0 °C(Predicted) | [density ]
1.144±0.06 g/cm3(Predicted) | [storage temp. ]
Store at -20°C | [solubility ]
DMSO : 250 mg/mL (858.10 mM; Need ultrasonic) | [form ]
Solid | [pka]
16.02±0.30(Predicted) | [color ]
White to off-white |
| Hazard Information | Back Directory | [Uses]
XST-14 is a potent, competitive and highly selective ULK1 inhibitor with an IC50 of 26.6 nM. XST-14 induces autophagy inhibition by reducing the phosphorylation of the ULK1 downstream substrate. XST-14 induces apoptosis in hepatocellular carcinoma (HCC) cells and has antitumor effects[1]. | [Biological Activity]
XST-14 is a potent, competitive and highly selective ULK1 inhibitor with an IC50 of 26.6 nM. XST-14 induces autophagy inhibition by reducing the phosphorylation of the ULK1 downstream substrate. XST-14 induces apoptosis in hepatocellular carcinoma (HCC) cells and has antitumor effects[1].
XST-14 inhibits ULK1 (IC50=13.6 nM), MAP2K1/MEK1 (IC50=721.8 nM), MAPK14/p38 alpha (IC50=283.9 nM), TGFBR2 (IC50=809.3 nM), ACVR1/ALK2 (IC50=183.8 nM), ULK2 (IC50=70.9 nM) and CAMK2A (IC50=66.3 nM) by the 10-point titration results from SelectScreen Kinase Profiling Services[1]. XST-14 (20-80 μM; for 24 h) leads a decrease in cell proliferation activity[1]. XST-14 (5 μM; for 24 h) induces apoptosis in HepG2 and human primary HCC cells[1]. XST-14 (5 μM; for 12 h) strongly inhibits the conversion of LC3-I to LC3-II in CHO cells stably expressing GFP-LC3[1]. XST-14 (5 μM; for 12 h) inhibits the Ser249 phosphorylation of PIK3C3 and Ser15 phosphorylation of BECN1[1].
XST-14 (15, 30 mg/kg/day; IP; for 4 consecutive weeks) displays anti-HCC efficacies, resulting in decreased tumor weights and suppressed tumor growth of HCC cells in nude mice[1]. XST-14 (2 mg/kg for IV; 10 mg/kg for IP) has a T1/2 of 2.31 hours for IV and a T1/2 of 2.69 hours for IP[1]. | [in vivo]
XST-14 (15, 30 mg/kg/day; IP; for 4 consecutive weeks) displays anti-HCC efficacies, resulting in decreased tumor weights and suppressed tumor growth of HCC cells in nude mice[1].
XST-14 (2 mg/kg for IV; 10 mg/kg for IP) has a T1/2 of 2.31 hours for IV and a T1/2 of 2.69 hours for IP[1].
| Animal Model: | Nude mice bearing HepG2 tumor xenografts[1] | | Dosage: | 15, 30 mg/kg | | Administration: | IP; daily; for 4 consecutive weeks | | Result: | Displayed anti-HCC efficacies, resulting in decreased tumor weights and suppressed tumor growth of HCC cells in nude mice.
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| Animal Model: | Sprague-Dawley rat[1] | | Dosage: | 2 mg/kg for IV; 10 mg/kg for IP (Pharmacokinetic Analysis) | | Administration: | IV or IP | | Result: | Had a T1/2 of 2.31 hours, a CL of 26.28 mL/min?kg, and and an AUC of 1269 hr?ng/mL for IV.
Had a T1/2 of 2.69 hours, a Cmax of 2033 ng/mL, and an AUC of 5979 hr?ng/mL for IP.
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| [IC 50]
CaMK II; ULK1: 26.6 nM (IC50) | [References]
[1]. Si-Tu Xue, et al. The role of the key autophagy kinase ULK1 in hepatocellular carcinoma and its validation as a treatment target . Autophagy. 2020 Oct;16(10):1823-1837. |
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