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商品描述
HG-9-91-01
- Catalog No.：MC1374
- Data Sheet
- MSDS
- Support
- Description
- References ( 0 )
- Protocol
- CasNo：
- 1456858-58-4
- MolecularFormula：
- C32H37N7O3
- Purity：
- >98%
- Target：
- Salt-inducible Kinase (SIK)
- IC50：
- IC50: 0.92/6.6/9.6 nM (SIK1/2/3)[1]
- In Vitro：
- HG-9-91-01 inhibits a number of protein tyrosine kinases that possess a threonine residue at the gatekeeper site, such as Src family members (Src, Lck, and Yes), BTK, and the FGF and Ephrin receptors[1]. HG-9-91-01 demonstrates a strong correlation between the potency of SIK2 inhibition and enhanced IL-10 production. In agreement with these reports, pretreating BMDCs with HG-9-91-01, a recently described inhibitor of SIK1-3, along with several other kinases, results in concentration-dependent potentiation of zymosan-induced IL-10 production with an EC50 ∼ 200 nM and a maximum effect similar to that observed with PGE2[2]. HG-9-91-01 has more than a 100-fold greater potency against SIKs than AMPK (IC50=4.5 μM) in a cell-free assay. HG-9-91-01 treatment dose dependently increased mRNA expression of Pck1 and G6pc and that effect is similar in cells treated with 4 μM HG-9-91-01 or 0.1 μM glucagon. Consistent with this observation, there is also a dose-dependent increase in glucose productio
- Fields：
- HG-9-91-01 is a potent and highly selective salt-inducible kinase (SIKs) inhibitor with IC50s of 0.92 nM, 6.6 nM and 9.6 nM for SIK1, SIK2 and SIK3 respectively.
- Specificity：
- Target: Salt-inducible Kinase (SIK). Fields: HG-9-91-01 is a potent and highly selective salt-inducible kinase (SIKs) inhibitor with IC50s of 0.92 nM, 6.6 nM and 9.6 nM for SIK1, SIK2 and SIK3 respect
- Source：
- Rabbit
- Dilution：
- IC50: 0.92/6.6/9.6 nM (SIK1/2/3)[1]
- Concentration：
- >98%
- Storage Stability：
- 2 years -20°C Powder, 2 weeks4°C in DMSO,6 months-80°C in DMSO
- Other Name：
- SIK inhibitor 1
- MolecularWeight(Da)：
- 567.6799999999999
- References：
- [1]. Clark K, et al. Phosphorylation of CRTC3 by the salt-inducible kinases controls the interconversion of classically activated andregulatory macrophages. Proc Natl Acad Sci U S A. 2012 Oct 16;109(4
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