Tissue-signaling research
LL-37
Lyophilized immune-signaling research peptide for pathway review
LL-37 is a cathelicidin antimicrobial peptide used in host-defense, epithelial barrier, immune, and inflammation research.
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Get catalog updatesFor laboratory research use only. Not for human or veterinary use. Not intended to diagnose, treat, cure, mitigate, or prevent disease.
Keep sealed, cold, dry, and protected from heat swings. Confirm product-specific storage on arrival.
Packed for transit stability with order support available for warm-weather routes.
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研究背景
LL-37 研究プロファイル
LL-37 is the active human cathelicidin peptide studied as part of innate host-defense biology. Research spans direct antimicrobial activity, membrane interaction, biofilm response, epithelial repair, chemotaxis, immune signaling, and inflammatory regulation. Its behavior is highly context dependent: concentration, salt conditions, cell type, microbial species, and assay design can shift results from protective signaling to cytotoxic or pro-inflammatory effects. LL-37 is best selected when a project needs the defined human cathelicidin sequence for antimicrobial, epithelial, or innate-immune comparisons. Because this is a potent amphipathic peptide, published activity should not be generalized across assay systems or interpreted as personal-use guidance.
想定される機序
An amphipathic human cathelicidin that can disrupt microbial membranes and also interact with host membranes, nucleic acids, formyl-peptide receptors, purinergic receptors, and inflammatory signaling networks. Its activity is strongly concentration and environment dependent.
研究で報告された作用
- In vitro studies report antibacterial, antiviral, antifungal, and antibiofilm activity against selected organisms and assay conditions.
- Cell and animal models report chemotaxis, epithelial migration, angiogenesis, wound-related effects, and modulation of innate immune responses.
- At higher concentrations or in susceptible systems, LL-37 can be cytotoxic, pro-inflammatory, or promote unwanted cell signaling.
一般的な研究エンドポイント
Minimum inhibitory concentration, membrane permeabilization, biofilm mass, chemotaxis, cytokines, epithelial closure, angiogenesis, cell viability, hemolysis, and receptor signaling.
エビデンスと限界
The mechanistic literature is extensive but highly context dependent. Assay conditions strongly limit comparison, and human therapeutic conclusions are not established for catalog material.
External reading
Literature for context—not product proof.
Third-party sources describe their own research materials and methods. They do not validate a specific Azure catalog batch.
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