SIRT5-IN-10
SIRT5-IN-10 is a competitive SIRT5 inhibitor. SIRT5-IN-10 improves renal function and reduces histopathological damage in septic acute kidney injury (AKI) mice. SIRT5-IN-10 can be used for the research of sepsis-associated AKI.
For research use only. We do not sell to patients.
- Formula: C27H30N8O7S
- Molecular Weight:610.64
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Storage:
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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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
SIRT5 |
In Vitro
SIRT5-IN-10 (compound 56) (0.03-600 μM; 2 h) potently inhibits recombinant human SIRT5 catalytic domain with an IC50 of 0.29 μM at 100 μM NAD+ and 0.79 μM at 400 μM NAD+[1].
SIRT5-IN-10 acts as a dual competitive inhibitor of recombinant human SIRT5, competing for binding with both the NAD+ cofactor and the P16 substrate[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
| Species | Dose | Route | AUC0-∞ | Cmax | Tmax | T1/2 | Vz | CL | AUC0-24 |
|---|---|---|---|---|---|---|---|---|---|
| Rat[1] | 10 mg/kg | i.p. | 1601.71 ng/mL·h | 417.39 ng/mL | 0.69 h | 2.75 h | 73560 mL/kg | 6330 mL/h/kg | 1487.85 ng·h/mL |
In Vivo
SIRT5-IN-10 (40 mg/kg; i.p.; two doses (1 h pre-LPS injection and 8 h post-LPS (HY-D1056) injection)) significantly protects against LPS-induced septic AKI in mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J mice (male, 8 weeks old) with CLP-induced septic AKI[1]
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Dosage:20; 40 mg/kg
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Administration:i.p.; two doses (1 h pre-surgery and 8 h post-surgery)
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Result:Reduced serum blood urea nitrogen (BUN) and serum creatinine (Scr) levels at 40 mg/kg dose.
Mitigated tubular dilation and damage via H&E staining and tubular injury scoring at 40 mg/kg dose.
Downregulated renal mRNA expression of injury markers Havcr1 (KIM-1) and Lcn2 (NGAL) at 40 mg/kg dose.
Exhibited renoprotective effects at both doses, with 40 mg/kg being more potent.
Showed no statistically significant differences in serum ALT, AST, Scr, or BUN levels between compound-treated mice and normal controls.
Caused no notable histopathological changes in heart, liver, lung, spleen, or testis tissues.
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Animal Model:C57BL/6J mice (male, 8 weeks old) with LPS-induced septic AKI[1]
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Dosage:40 mg/kg
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Administration:i.p.; two doses (1 h pre-LPS injection and 8 h post-LPS injection)
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Result:Attenuated LPS-induced elevations in serum Scr and BUN levels.
Downregulated renal mRNA expression of KIM-1 and NGAL.
Ameliorated histopathological renal damage.
Partially normalized aberrant renal succinylation profiles.
Suppressed pro-inflammatory JAK-STAT signaling by reducing renal mRNA expression of Il6, Jak1, Jak2, and Stat3.
Lowered plasma CRP levels.
Decreased renal mRNA levels of inflammatory mediators Il6, Mcp1, and Tnf-α.
Chemical Information
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Molecular Weight 610.64
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Formula C27H30N8O7S
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SMILES
O=C(C1=C(N=C(N=C1)C2=CC=C(S2)C(C)=O)NCCCN/C(NCCC(O)=O)=C\[N+]([O-])=O)NC3=CC=CC(NC(C)=O)=C3
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Nephrotoxicity Study
This protocol assesses nephrotoxicity by combining functional kidney injury readouts, urinary/tissue injury biomarkers, and renal histopathology. Serum creatinine and BUN reflect impaired kidney function, while KIM-1, NGAL, clusterin, osteopontin, IL-18, cystatin C, nephrin, Oat5, urinary protein, glucose, and alkaline phosphatase have been used to detect tubular injury in cisplatin-, gentamicin-, and acetaminophen-induced nephrotoxicity models.
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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.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
SIRT5-IN-10 Related Classifications
HY-184000 Related Classifications
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