Gallinamide A TFA
Based on 1 Customer Validation
Gallinamide A TFA is a linearly depositing peptide and a potent inhibitor of cathepsin L (CatL) (IC50: 17.6 pM). Gallinamide A TFA inhibits SARS-CoV-2 infection by inhibiting CatL (EC50: 28 nM). Gallinamide A TFA also inhibits Plasmodium falciparum (IC50: 50 nM).
For research use only. We do not sell to patients.
- Purity : 99.85%
- CAS No.: 1352920-57-0
- Formula: C33H53F3N4O9
- Molecular Weight:706.79
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Storage:
4°C, protect from light, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light, stored under nitrogen)
Biological Activity
Description
IC50 & Target
IC50: 17.6 pM (Cathepsin L); 7.34 nM (Cathepsin B); 697 nM (Cathepsin V); 79.6 nM (Cathepsin K); 367 pM (Cathepsin S)[1]
EC50: 28 nM (SARS-CoV-2)[1]
IC50: 50 nM (P. falciparum)[2]
In Vitro
Gallinamide A TFA has low cytotoxicity with CC50 >100 μM in VeroE6 cells. Gallinamide A TFA (0.5 μM; 96 h) can inhibit CatL-mediated SARS-CoV-2 endosome entry into VeroE6 cells[1].
Gallinamide A TFA also mesylate with the TMPRSS2 inhibitor Nafamostat (HY-B0190A) exhibits synergistic effects. Potent antiviral activity in HEK-ACE2-TMPRSS2 cells, but ineffective in VeroE6 cell line[1].
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. 1352920-57-0
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Appearance Solid
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Molecular Weight 706.79
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Formula C33H53F3N4O9
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Color White to off-white
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SMILES
CC[C@H](C)[C@H](N(C)C)C(O[C@@H](CC(C)C)C(N[C@@H](CC(C)C)C(N[C@@H](C)/C=C/C(N1[C@H](C(OC)=CC1=O)C)=O)=O)=O)=O.OC(C(F)(F)F)=O
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Structure Classification
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Initial Source
marine cyanobacterium Schizothrix sp.
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
4°C, protect from light, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light, stored under nitrogen)
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.
Purity & Documentation
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Data Sheet (269 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
[1]. Ashhurst AS, et al. Potent in vitro anti-SARS-CoV-2 activity by gallinamide A and analogues via inhibition of cathepsin L. bioRxiv [Preprint]. 2020 Dec 24:2020.12.23.424111. [Content Brief]
[2]. Stoye A, et al. Falcipain Inhibitors Based on the Natural Product Gallinamide A Are Potent in Vitro and in Vivo Antimalarials. J Med Chem. 2019 Jun 13;62(11):5562-5578. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)