[CAS NO. 1456858-58-4] HG-9-91-01
PRODUCTS SPECIFICATIONS [1456858-58-4]
DESCRIPTION [1456858-58-4]
Overview
| MDL | - |
|---|---|
| Molecular Weight | 567.68 |
| Molecular Formula | C32H37N7O3 |
| SMILES | CC1=CC=CC(C)=C1NC(N(C2=NC=NC(NC3=CC=C(N4CCN(C)CC4)C=C3)=C2)C5=CC=C(OC)C=C5OC)=O |
19 Publications Citing Use of MCE
- [1]Cell Rep. 2017 Jun 13;19(11):2177-2184.
- [2]Oncogene. 2022 Mar 11.
- [3]Elife. 2015 Nov 17;4:e08501.
- [4]Cell Death Dis. 2022 Feb 25;13(2):188.
- [5]Cell Death Dis. 2020 Jan 13;11(1):25.
- [6]Cell Death Dis. 2019 Oct 31;10(11):826.
- [7]JCI Insight. 2022 May 10;e150363.
- [8]J Cell Sci. 2021 Aug 5;jcs.258685.
- [9]Inflamm Bowel Dis. 2021 May 14;izab072.
- [10]J Biol Chem. 2015 Jul 17;290(29):17879-93.
- [11]Cell Signal. 2020 Dec;76:109786.
- [12]J Gen Physiol. 2019 Feb 4;151(2):264-272.
- [13]Biochem Biophys Res Commun. 2019 Jan 15;508(3):775-779.
- [14]Heliyon. 10 October 2022, e11016.
- [15]Nature Metabolism. 2021 May;3(5):682-700.
- [16]Patent. US20200246435A1.
- [17]bioRxiv. 2020 Apr.
- [18]Technical University of Munich. 2017 Oct.
- [19]Kansai University. 2017 Mar.
Summary
HG-9-91-01 is a potent and highly selective salt-inducible kinase ( SIK ) inhibitor with IC 50 s of 0.92 nM, 6.6 nM and 9.6 nM for SIK1 , SIK2 and SIK3 respectively.
IC50 & Target
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 EC 50 ~200 nM and a maximum effect similar to that observed with PGE 2 [2] . HG-9-91-01 has more than a 100-fold greater potency against SIKs than AMPK (IC 50 =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. Consistent with this observation, there is also a dose-dependent increase in glucose production following HG-9-91-01 treatment [3] .
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Appearance
Solid
Shipping
Room temperature in continental US; may vary elsewhere.
Storage
| Powder | -20°C | 3 years |
|---|---|---|
| 4°C | 2 years | |
| In solvent | -80°C | 6 months |
| -20°C | 1 month |
Solvent & Solubility
DMSO : ≥ 150 mg/mL ( 264.23 mM )
* "≥" means soluble, but saturation unknown.
Stock Solutions
| Concentration Solvent Mass | 1 mg | 5 mg | 10 mg |
|---|
| 1 mM | 1.7616 mL | 8.8078 mL | 17.6156 mL |
| 5 mM | 0.3523 mL | 1.7616 mL | 3.5231 mL |
| 10 mM | 0.1762 mL | 0.8808 mL | 1.7616 mL |
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(42):16986-91.
- [2] Sundberg TB, et al. Small-molecule screening identifies inhibition of salt-inducible kinases as a therapeutic strategy to enhance immunoregulatory functions of dendritic cells. Proc Natl Acad Sci U S A. 2014 Aug 26;111(34):12468-73.
- [3] Patel K, et al.The LKB1-salt-inducible kinase pathway functions as a key gluconeogenic suppressor in the liver. Nat Commun. 2014 Aug 4;5:4535.