DPP9-IN-2
DPP9-IN-2 is a selective, potent and orally active inhibitor of Dipeptidyl Peptidase 9 (DPP9 ) with an IC50 of 12.9 nM. DPP9-IN-2 shows a SI of 59 over DPP8, and shows no significant inhibitory activity against related peptidases including DPP2, DPP4, FAP, and PREP. DPP9-IN-2 can induce cancer cells pyroptosis and has weak synergistic anti-HIV-1 activity when combined with non-nucleoside reverse transcriptase inhibitor. DPP9-IN-2 can be used for the researches of cance rand infection.
For research use only. We do not sell to patients.
- CAS No.: 3020859-44-0
- Formula: C33H33F2N3O2
- Molecular Weight:541.63
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
DPP-9 12.9 nM (IC50) |
HIV-1 |
In Vitro
DPP9-IN-2 (Compound 6e) (0.05-5 μM; 24-48 h) induces pyroptosis in THP-1 cells, promoting LDH release and SYTOX Green uptake [1].
DPP9-IN-2 (0.5-5 μM; 24 h) induces pyroptosis depending on DPP9, CASP1, and GSDMD, and pyroptosis is significantly inhibited or delayed in DPP9-knockdown, CASP1-KO, or GSDMD-KO THP-1 cells[1].
DPP9-IN-2 (5 μM) shows weak synergistic anti-HIV-1 activity when combined with non-nucleoside reverse transcriptase inhibitors (Efavirenz (HY-10572), Rilpivirine (HY-10574)) in MT-4 cells[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 | Note | F | AUC0-last | Cl | Vd | T1/2 |
|---|---|---|---|---|---|---|---|---|
| Rat | 20 mg/kg | p.o. | 文献审核 | 61 % | 8176.1 ng·h/mL | / | / | / |
| Rat | 5 mg/kg | i.v. | 文献审核 | / | 3368.3 ng·h/mL | 1.5 L/h/kg | 23 L/kg | 10.9 h |
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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CAS No. 3020859-44-0
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Molecular Weight 541.63
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Formula C33H33F2N3O2
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SMILES
O=C(C1=CC=C(C2=CC=C(F)C=C2)C=C1)NC34CC5(NCC(N6CC7=C(C=C(F)C=C7)C6)=O)CC(C4)CC(C5)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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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
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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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Pyroptosis Solutions
Pyroptosis is a lytic inflammatory cell-death pathway executed by gasdermin pores, most classically through inflammasome-mediated activation of caspase-1, cleavage of gasdermin D, membrane pore formation, LDH release, and secretion of IL-1β and IL-18. The canonical pathway is commonly modeled by priming cells with an inflammatory signal such as LPS to induce pro-IL-1β and inflammasome components, followed by an activation signal such as ATP or nigericin to activate NLRP3, ASC speck formation, caspase-1 cleavage, GSDMD cleavage, cytokine release, and pyroptotic membrane rupture. The non-canonical pathway is triggered when cytosolic LPS activates mouse caspase-11 or human caspase-4/5, leading to GSDMD cleavage and pyroptosis, and this can secondarily activate NLRP3-dependent IL-1β release. Pyroptosis is linked to inflammatory injury, infection, cancer, liver disease, ocular disease, placental inflammation, and other disease phenotypes, but unresolved questions include which gasdermin fam
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)