HPA-IN-3
HPA-IN-3 (compound 5) is a heparanase (HPA) inhibitor with an IC50 of 11.27 μM against human targets. HPA-IN-3 binds to the active site of HPA, and its structural features enhance binding stability and affinity. HPA-IN-3 reduces the levels of proinflammatory cytokines. HPA-IN-3 maintains organ morphology. HPA-IN-3 improves the survival rate of mice with sepsis induced by cecal ligation and puncture. HPA-IN-3 can be used in studies related to sepsis.
For research use only. We do not sell to patients.
- Formula: C25H32N2Na10O45S8
- Molecular Weight:1566.93
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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]|
hHPA 11.27 μM (IC50) |
In Vitro
HPA-IN-3 (compound 5) (0-1000 μM; 10 min pre-incubation with HPA, 30 min incubation with substrate) potently inhibits recombinant active heparanase with an IC50 of 11.27 μM[1].
HPA-IN-3 (0-10000 μM; 3 min) shows minimal interference with the intrinsic coagulation cascade, with no significant aPTT prolongation observed at concentrations up to 10000 μM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J (male, 6-8 weeks old, 20-25 g, CLP-induced sepsis model)[1]
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Dosage:40 mg/kg
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Administration:s.c.; single dose
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Result:Achieved a 60% survival rate over 120 hours.
Reduced serum levels of TNF-α, IL-6, and IL-1β.
Decreased inflammatory infiltrates and preserved tissue architecture in lung and kidney tissues.
Lowered lung and kidney injury scores significantly relative to the CLP control group.
Chemical Information
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Molecular Weight 1566.93
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Formula C25H32N2Na10O45S8
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SMILES
O[C@@H]1[C@@H](OS(=O)(O[Na])=O)[C@H](OS(=O)(O[Na])=O)[C@@H](C(O[Na])=O)O[C@H]1O[C@H]2[C@H](COS(=O)(O[Na])=O)OC(OC3[C@H](C(O[Na])=O)OC(O[C@H]4C(O)[C@@H](NS(=O)(O[Na])=O)[C@@H](OC)O[C@@H]4COS(=O)(O[Na])=O)[C@H](OS(=O)(O[Na])=O)[C@H]3O)[C@@H](NS(=O)(O[Na])=O)[C@@H]2OS(=O)(O[Na])=O
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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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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.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
HPA-IN-3 Related Classifications
HY-184684 Related Classifications
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