Papiliocin
Papiliocin is a potent peptide antibiotic with both anti-inflammatory and antibacterial activities. Papiliocin is primarily active against Gram-negative bacteria. Papiliocin exhibits strong anti-inflammatory activity against cell, exerting its anti-inflammatory activity by inhibiting the production of NO and the secretion of TNF-α and MIP-2. Papiliocin participates in the innate defense response mechanism by inhibiting the Toll-like receptor pathway and NF-κB. Papiliocin induces apoptosis in fungal cells and increases the total level of intracellular ROS. Papiliocin acts as an effective antiseptic peptide in sepsis models. Papiliocin is useful in anti-inflammatory and antibacterial research.
For research use only. We do not sell to patients.
- Formula: C183H314N56O44
- Molecular Weight:4002.80
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
All Antibiotic Isoforms
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Biological Activity
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IL-1β |
IL-6 |
TLR4 |
iNOS |
Papiliocin (37 °C for 16 h) shows antibacterial activity against Gram-negative species (E. coli, S. typhimurium, and P. aeruginosa) and Gram-positive species (B. subtilis, S. epidermidis, and S. aureus), with MICs of 0.25, 0.5, 1, 16, 2, 32 μM[1].
Papiliocin is calcium- and magnesium-tolerant to Gram-negative bacteria[1].
Papiliocin (0-100 μM, 37 °C for 1 h) lacks hemolytic activity and is not cytotoxic to RAW264.7 cells, with an IC50 of 58 μm[1].
Papiliocin (0-25 μM, 3-24 h) inhibits the expression of NO, TNF-α, MIP-2, iNOS, TLR4, NF-κB, and all inflammatory cytokines IL-1β, IL-6, MIP-1, MIP-2, and TNF-α genes in LPS (HY-D1056)-stimulated RAW264.7 cells[1].
Papiliocin (0-10 μM) induces lipid vesicle permeabilization, shows low Stern-Volmer quenching constants (KSV) in micelles or SUVs, results in the dissociation of LPS aggregates through interaction with LPS[1].
Papiliocin (30 μM, 28 °C for 2 h) induces ROS production and increases intracellular hydroxyl radical levels in Candida albicans cells[2].
Papiliocin (30 μM, 28 °C for 2 h) induces apoptotic cell death, membrane depolarization and metacaspase activation, DNA damage in Candida albicans cells[2].
Papiliocin (0-50 μM) displaces 74.6% of the BC probes from LPS, neutralizes LPS, with the binding affinity of 0.063 μM[3].
Papiliocin (40 μM, 30 min) inhibits 52% of FITC-LPS binding to the surface of RAW 264.7 cells, but also competitively displaces 25% of pre-bound LPS from the LPS-receptor complex on RAW 264.7 cells[3].
Papiliocin (0-100 μM) reduces TLR4-mediated SEAP activity with an IC50 of 1.1 μM[3].
Papiliocin (0.1-10 μM, 1 h) blocks the LPS-induced inflammatory cascade by targeting TLR4 and the MAPK pathway and by blocking the nuclear translocation of p-NF-κB in RAW 264.7 cells[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:LPS (20 ng/mL)-stimulated RAW264.7 cells
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Concentration:1, 10 μM
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Incubation Time:18 h
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Result:Inhibited the production of TNF-α and MIP-2.
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Cell Line:LPS (20 ng/mL)-stimulated RAW264.7 cells
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Concentration:20 μM
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Incubation Time:3 h
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Result:Inhibited the expression of iNOS and all inflammatory cytokines, including IL-1β, IL-6, MIP-1, MIP-2, and TNF-α.
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Cell Line:LPS (20 ng/mL)-stimulated RAW264.7 cells
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Concentration:25 μM
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Incubation Time:24 h
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Result:Inhibited TLR4 and NF-κB expression and prevented the translocation of NF-κB from the cytoplasm to the nucleus.
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Cell Line:Candida albicans cells
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Concentration:30 μM
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Incubation Time:28 °C for 2 h
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Result:Induced apoptosis cell death, with the early apoptotic cells of 61.14%, the late apoptotic of 0.52%.
Induced the breakdown of ΔΨm and the loss of mitochondrial permeability.
Induced the generation of strong oxidant hydroxyl radicals.
Increased the proportion of TUNEL-positive cell nuclei.
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Cell Line:LPS (50 ng/mL)-stimulated RAW264.7 cells
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Concentration:0.1, 0.5, 1 μM
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Incubation Time:1 h
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Result:Reduced MyD88 overexpression and phosphorylation levels of TAK1, p38, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK).
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Cell Line:LPS (50 ng/mL)-stimulated RAW264.7 cells
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Concentration:10 μM
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Incubation Time:1 h
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Result:Reduced expression of Alexa 546 inhibited Lp-NF-κB p65 translocation.
Chemical Information
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Molecular Weight 4002.80
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Formula C183H314N56O44
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Sequence
Arg-Trp-Lys-Ile-Phe-Lys-Lys-Ile-Glu-Lys-Val-Gly-Arg-Asn-Val-Arg-Asp-Gly-Ile-Ile-Lys-Ala-Gly-Pro-Ala-Val-Ala-Val-Val-Gly-Gln-Ala-Ala-Thr-Val-Val-Lys-NH2
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Sequence Shortening
RWKIFKKIEKVGRNVRDGIIKAGPAVAVVGQAATVVK-NH2
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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.
Purity & Documentation
References
[1]. Kim JK, et al. Structure and function of papiliocin with antimicrobial and anti-inflammatory activities isolated from the swallowtail butterfly, Papilio xuthus. J Biol Chem. 2011 Dec 2;286(48):41296-41311. [Content Brief]
[2]. Hwang B, et al. Induction of yeast apoptosis by an antimicrobial peptide, Papiliocin. Biochem Biophys Res Commun. 2011 Apr 29;408(1):89-93. [Content Brief]
[3]. Krishnan M, et al. Molecular mechanism underlying the TLR4 antagonistic and antiseptic activities of papiliocin, an insect innate immune response molecule. Proc Natl Acad Sci U S A. 2022 Mar 8;119(10):e2115669119. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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