RIPK2-IN-8
RIPK2-IN-8 is an orally active and highly selective RIPK2 inhibitor (IC50 = 11 nM). RIPK2-IN-8 is highly selective for RIPK2 over RIPK1 (IC50 > 30,000 nM) and has a moderate inhibitory effect on RIPK3 (IC50 = 44.61 nM). RIPK2-IN-8 inhibits the NOD2-RIPK2 signaling pathway and the expression of the inflammatory cytokines IL-6 and TNFα, thereby exerting anti-inflammatory effects. RIPK2-IN-8 has demonstrated anti-inflammatory and hepatoprotective effects in an acute liver injury (ALI) model and can be used in ALI research.
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- CAS. Nr.: 3036254-29-9
- Formel: C22H20FN5OS2
- Molecular Weight:453.56
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biologische Aktivität
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Chemical Information
- Protokoll
- Reinheit & Dokumentation
- Verweise
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Help & FAQs
Biologische Aktivität
Beschreibung
IC50 & Target
[1]|
RIPK2 11 nM (IC50) |
RIPK3 44.61 nM (IC50) |
IL-6 |
In Vitro
RIPK2-IN-8 (Compound HY3)(0-10 μM, 0.5-6 h) delays NF-kB and MAPK activation without affecting protein expression or cell viability in L18-MDP (HY-148690)-stimulated THP-1 cells[1].
RIPK2-IN-8 (1 μM) shows almost no inhibitory activity against inflammation-related kinases, such as BTK, FLT3, JNK2α2, SAPK3, MSK1, MAPKAP-K2[1].
RIPK2-IN-8 has weak cytotoxicity against H9C2 cells(IC50 > 40 μM)[1].
RIPK2-IN-8 inhibits IL-8 production with an IC50 of 29 nM in Muramyl dipeptide (MDP) (HY-127090)-stimulated THP-1 cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:THP-1 cells were stimulated with L18-MDP
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Concentration:0 μM, 0.001 μM, 0.003 μM, 0.01 μM, 0.03 μM, 0.1 μM, 0.3 μM, 1 μM, 3 μM, 10 μM
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Incubation Time:0.5 h, 6 h
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Result:Delayed phosphorylation of p65, p38, and JNK. At 1 μM, did not alter the total levels of p65, p38, JNK, and β-actin.
Did not affect phosphorylation of RIPK3 or MLKL, key markers of necroptotic signaling.
Parmacokinetics
In Vivo
RIPK2-IN-8 (5-20 mg/kg, p.o., once) exerts a liver-protective effect by inhibiting the expression of inflammatory cytokines, thereby reducing serum inflammatory markers and alleviating liver damage in Acetaminophen (APAP) (HY-66005)-induced ALI model[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:MDP-induced (100 μg, i.p.) peritonitis mice (Female C57BL/6 at 8 weeks of age) model[1]
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Dosage:7.5 mg/kg, 15 mg/kg, 30 mg/kg
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Administration:p.o., once
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Result:Reduced IL-6 levels, with IL-6 levels dropping to 23.9 pg/mL at 30 mg/kg, comparable to the RIPK2-positive compound GSK2983559 (HY-112038A).
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Animal Model:APAP-induced (500 mg/kg, i.p.) ALI mice (Female C57BL/6 at 8 weeks of age) model[1]
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Dosage:5 mg/kg, 10 mg/kg, 20 mg/kg
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Administration:p.o., once
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Result:Reduced ALT and AST levels, particularly in the high-dose group, where ALT and AST levels decreased to 202 and 275 U/L, respectively.
Reduced serum and mRNA levels of IL-6 and TNFα.
Chemical Information
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CAS. Nr. 3036254-29-9
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Molecular Weight 453.56
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Formel C22H20FN5OS2
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SMILES
CCC(NC1CCC(C2=CC(N=CN=C3NC4=CC(N=CS5)=C5C=C4F)=C3S2)=CC1)=O
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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LPS-Induced Endotoxemia/Systemic Inflammation
Lipopolysaccharide (LPS)-induced endotoxemia is a widely used in vivo model of acute systemic inflammation in which LPS, a Gram-negative bacterial endotoxin, activates innate immune signaling primarily through TLR4, leading to rapid and transient induction of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β in circulation and tissues. This cytokine surge is commonly used as a measurable readout of systemic inflammatory activation and immune dysregulation, and is typically assessed within hours after intraperitoneal LPS administration in mouse models of endotoxemia. The model captures key features of systemic inflammatory response syndrome, including cytokine release, immune cell activation, and downstream tissue responses, and has been used to evaluate anti-inflammatory interventions such as cytokine modulation, lipid mediators, and immune cell-targeting therapies.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Reinheit & Dokumentation
Verweise
[1]. Zhao H, et al. Development of Thieno[3,2-d]pyrimidine derivatives as potent RIPK2 inhibitors with Prominent In vitro and In vivo anti-inflammatory efficacy. Eur J Med Chem. 2025 Jul 5;297:117932. [Content Brief]
[2]. Zhao H, et al. Development of Thieno[3,2-d]pyrimidine derivatives as potent RIPK2 inhibitors with Prominent In vitro and In vivo anti-inflammatory efficacy. Eur J Med Chem. 2025 Jul 5;297:117932. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
RIPK2-IN-8 Related Classifications
HY-175026 Related Classifications
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