| Chemical Properties | Back Directory | [storage temp. ]
Store at -20°C | [solubility ]
DMSO : 10 mg/mL (23.81 mM; ultrasonic and warming and heat to 60°C)| | [form ]
Solid | [color ]
Yellow to brown | [Water Solubility ]
Water : 2.5 mg/mL (5.95 mM; ultrasonic and warming and heat to 60°C) |
| Hazard Information | Back Directory | [Uses]
GSK-872 hydrochloride is a RIPK3 inhibitor, which binds RIP3 kinase domain with an IC50 of 1.8 nM, and inhibits kinase activity with an IC50 of 1.3 nM. GSK-872 hydrochloride decreases the RIPK3-mediated necroptosis and subsequent cytoplasmic translocation and expression of HMGB1, as well as ameliorates brain edema and neurological deficits in early brain injury[1][2][3]. | [Biological Activity]
GSK-872 hydrochloride is a RIPK3 inhibitor, which binds RIP3 kinase domain with an IC50 of 1.8 nM, and inhibits kinase activity with an IC50 of 1.3 nM. GSK-872 hydrochloride decreases the RIPK3-mediated necroptosis and subsequent cytoplasmic translocation and expression of HMGB1, as well as ameliorates brain edema and neurological deficits in early brain injury[1][2][3].
GSK-872 (GSK’872; 0.01-3 μM; 24 hours) blocks TNF-induced necroptosis in human HT-29 cells in a concentration-dependent manner[1].
GSK-872 hydrochloride (25 mM; intracerebroventricular injection) can attenuate brain edema and improve neurological function following subarachnoid hemorrhage (SAH) and reduce the number of necrotic cells. GSK-872 hydrochloride can also decrease the protein levels of RIPK3 and MLKL, and cytoplasmic translocation and expression of HMGB1, an important pro-inflammatory protein[3]. | [in vivo]
GSK-872 hydrochloride (25 mM; intracerebroventricular injection) can attenuate brain edema and improve neurological function following subarachnoid hemorrhage (SAH) and reduce the number of necrotic cells. GSK-872 hydrochloride can also decrease the protein levels of RIPK3 and MLKL, and cytoplasmic translocation and expression of HMGB1, an important pro-inflammatory protein[3]. | Animal Model: | Eight weeks old Sprague-Dawley male rats with 300-320 g body weight (rat SAH model)[3] | | Dosage: | 25 mM/6 μL | | Administration: | Syringe pump (intracerebroventricular) at 30 min after SAH | | Result: | Attenuated brain edema, improved neurological function and decreased the number of necrotic cells in the ipsilateral cortex. Decreased the expression of RIPK3, MLKL and cytoplasmic HMGB1 at 72 h after SAH in the ipsilateral cortex.
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| [IC 50]
RIPK3 | [References]
[1]. Mandal P, et al. RIP3 induces apoptosis independent of pronecrotic kinase activity. Mol Cell. 2014 Nov 20;56(4):481-95. [2]. Arora D, et al. Deltamethrin induced RIPK3-mediated caspase-independent non-apoptotic cell death in rat primary hepatocytes. Biochem Biophys Res Commun. 2016 Oct 14;479(2):217-223. [3]. Chen T, et al. Inhibiting of RIPK3 attenuates early brain injury following subarachnoid hemorrhage: Possibly through alleviating necroptosis. Biomed Pharmacother. 2018;107:563-570. |
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| Company Name: |
InvivoChem
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| Tel: |
13549236410 |
| Website: |
https://www.invivochem.cn/ |
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