D-Captopril
D-Captopril is a NDM-1 inhibitor and a competitive BlaB inhibitor, with an IC50 value of 21.8 µM against NDM-1 and a Ki of 70-100 µM against BlaB. D-Captopril synergistically reduces the minimum inhibitory concentration of Meropenem (HY-13678) against NDM-1-expressing bacteria. D-Captopril binds to BcII via its thiolate sulfur atom and carboxylate group, altering metal ion occupancy and modulating Cd2+ binding affinity. D-Captopril can be used in the research of neonatal meningitis, sepsis and bacterial infections.
For research use only. We do not sell to patients.
- CAS No.: 119238-52-7
- Formula: C9H15NO3S
- Molecular Weight:217.29
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[2]|
NDM-1 21.8 μM (IC50) |
In Vitro
D-Captopril (2 mM; ~5 weeks) binds to BlaB of *Chryseobacterium meningosepticum* by inserting its sulfhydryl group between the two active-site Zn2+ ions of BlaB and displacing the catalytic hydroxyl group. It acts as a competitive inhibitor of BlaB at neutral pH, with a Ki of 70-100 μM[1].
D-Captopril inhibits the enzymatic activity of purified wild-type NDM-1 through interactions with active site residues and stabilized water networks, with an IC50 value of 21.8 μM[2].
D-Captopril (8-32 mg/L) acts synergistically with Meropenem (HY-13678) at the concentration of 32 mg/L, reducing the MIC of Meropenem against E. coli DH5α expressing NDM-1 from 8 mg/L to 4 mg/L, whereas no synergistic effect is observed at the concentration of 8 mg/L[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 119238-52-7
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Molecular Weight 217.29
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Formula C9H15NO3S
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SMILES
SC[C@@H](C)C(N1[C@H](CCC1)C(O)=O)=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
[1]. García-Saez I, et al. The 1.5-A structure of Chryseobacterium meningosepticum zinc beta-lactamase in complex with the inhibitor, D-captopril. J Biol Chem. 2003;278(26):23868-23873. [Content Brief]
[2]. Ma G, et al. Structure-guided optimization of D-captopril for discovery of potent NDM-1 inhibitors. Bioorg Med Chem. 2021;29:115902. [Content Brief]
[3]. Heinz U, et al. Coordination geometries of metal ions in d- or l-captopril-inhibited metallo-beta-lactamases. J Biol Chem. 2003;278(23):20659-20666. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)