Cecropin A TFA
Based on 2 publication(s) in Google Scholar
Cecropin A TFA is a linear 37-residue antimicrobial polypeptide isolated from Hyalaphora cecropia pupae. Cecropin A TFA exhibits anti-bacterial, anti-inflammatory and anti-cancer activity.
For research use only. We do not sell to patients.
- Formula: C184H313N53O46.xC2HF3O2
- Molecular Weight:4003.78 (free base)
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Storage:
Sealed storage, away from moisture.
Powder -80°C, 2 years , -20°C, 1 year* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Publications Citing Use of MedChemExpress (MCE) Cecropin A TFA
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Biological Activity
Description
In Vitro
Cecropin A (10, 20, 30, 40 and 50 μM) induces cytotoxicity on HL-60 cells in a dose-dependent manner. Cecropin A induces apoptosis independent of caspase activation[1].
Cecropin A shows good antibacterial activity against both multidrug-resistant Gram-negative bacteria such as A. baumanii (MDRAB) and multidrug-resistant P. aeruginosa (MDRPA) with IC50s of 0.5-1 μM.
Cecropin A (0.1, 0.25 μM) exhibits anti-inflammatory activities. Cecropin A (25 μM) effectively suppresses the expression of mTNF-α, mIL-1β, and mMIP-2 mRNA and slightly inhibits the expression of mMIP-1 mRNA. Cecropin A also effectively inhibits LPS-induced phosphorylation of ERK, JNK, p38 MAPK, and reduced the expression of COX-2[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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Appearance Solid
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Molecular Weight 4003.78 (free base)
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Formula C184H313N53O46.xC2HF3O2
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Color White to off-white
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Sequence
Lys-Trp-Lys-Leu-Phe-Lys-Lys-Ile-Glu-Lys-Val-Gly-Gln-Asn-Ile-Arg-Asp-Gly-Ile-Ile-Lys-Ala-Gly-Pro-Ala-Val-Ala-Val-Val-Gly-Gln-Ala-Thr-Gln-Ile-Ala-Lys-NH2
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Sequence Shortening
KWKLFKKIEKVGQNIRDGIIKAGPAVAVVGQATQIAK-NH2
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Initial Source
Hyalaphora cecropia
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Sealed storage, away from moisture
Powder -80°C 2 years -20°C 1 year * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Publications (2)
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Journal Impact Factor
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Most Recent
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Cell Rep
Barceloneic acid A enables Metarhizium robertsii to establish parasitism in insects and mutualism in plants by inhibiting farnesyltransferase. [Abstract]2026 May 28;45(6):117371. PMID: 42213785 -
Probiotics Antimicrob Proteins
The Efficacy of Cecropin Against Multidrug-Resistant Bacteria Is Linked to the Destabilization of Outer Membrane Structure LPS of Gram-Negative Bacteria. [Abstract]2024 Dec 21. PMID: 39708190
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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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Purity & Documentation
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Data Sheet (283 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]. Cerón JM, et al. The antimicrobial peptide cecropin A induces caspase-independent cell death in human promyelocytic leukemia cells. Peptides. 2010 Aug;31(8):1494-503. [Content Brief]
[2]. Lee E, et al. Anti-inflammatory activities of cecropin A and its mechanism of action. Arch Insect Biochem Physiol. 2015 Jan;88(1):31-44. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)