W(Dab)L
W(Dab)L is a cationic membrane-disrupting antimicrobial peptide with protease stability, salt tolerance, and no induction of drug resistance. W(Dab)L is effective against planktonic MRSA, MRSA biofilms, and Pseudomonas aeruginosa, and exhibits low cytotoxicity to mammalian cells. As a bactericide, W(Dab)L selectively interacts with negatively charged bacterial membranes, triggering membrane permeabilization, deformation, disintegration, intracellular substance leakage, and ultimately leading to cell lysis. W(Dab)L maintains its chemical integrity and antimicrobial activity upon exposure to proteases and human serum. W(Dab)L can be used in studies of methicillin-resistant Staphylococcus aureus infections.
商品は「研究用試薬」です。人や動物の医療用・臨床診断用・食品用の製品ではありません。
研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- 分子式: C55H86N14O8
- 分子量:1071.36
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
生物活性
製品説明
体外実験
W(Dab)L (15-20 μM) inhibits planktonic MRSA growth with an MIC of 15 μM in salt-free conditions and 20 μM in the presence of physiological salts, displaying partial salt tolerance[1].
W(Dab)L (15 μM; up to 90 min) rapidly eliminates planktonic MRSA at its 15 μM MIC, achieving complete bacterial kill within 90 min[1].
W(Dab)L (15 μM) inhibits 95% of S. aureus (MRSA) biofilm growth at its MBIC of 15 μM[1].
W(Dab)L (30 μM) eradicates ~80% of 2-day mature S. aureus MRSA biofilms at its MBEC of 30 μM[1].
W(Dab)L (15-50 μM; 4 h) shows minimal hemolysis (<25%) of human RBCs at 50 μM and no hemolysis at its 15 μM MIC[1].
W(Dab)L (2.5-160 μM) is noncytotoxic to HeLa, HEK 293, and HDF cells at biologically active concentrations, with high cell survival observed even at concentrations up to 160 μM[1].
W(Dab)L (Sub-MIC concentrations; 30 days, 96 bacterial generations) does not induce resistance development in MRSA over 96 bacterial generations when exposed to sub-MIC concentrations[1].
W(Dab)L (15 μM; 6 h) remains stable after 6 h of incubation with a trypsin-chymotrypsin-proteinase K cocktail and retains full antimicrobial activity against MRSA with an MIC of 15 μM[1].
W(Dab)L (15 μM; 6 h) remains stable after 6 h of incubation in human serum and retains full antimicrobial activity against MRSA with an MIC of 15 μM[1].
W(Dab)L selectively interacts with bacterial membrane mimic SDS micelles (showing an 18 nm tryptophan fluorescence blue shift) and does not interact with mammalian membrane mimic DPC micelles[1].
W(Dab)L disrupts the S. aureus (MRSA) inner membrane, increasing PI fluorescence by 50% relative to Triton X-100 control, confirming membrane permeabilization[1].
W(Dab)L (15-30 μM) causes membrane deformation, blistering, and lysis of planktonic MRSA cells at 1× MIC (15 μM) and 2× MIC (30 μM), as observed via FESEM and TEM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
化学情報
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分子量 1071.36
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分子式 C55H86N14O8
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配列
Trp-{(Rac)-Dab}-Trp-Leu-{(Rac)-Dab}-{(Rac)-Dab}-Leu-Leu-NH2
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シーケンスの短縮
W-{(Rac)-Dab}-WL-{(Rac)-Dab}-{(Rac)-Dab}-LL-NH2
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
プロトコル
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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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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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Mammalian live/dead viability and cytotoxicity staining
Live/dead viability and cytotoxicity staining assays are based on the simultaneous detection of intracellular esterase activity in metabolically active (viable) cells and membrane integrity loss in non-viable cells. In commonly used dual-staining approaches, membrane-permeant fluorogenic substrates are converted by intracellular esterases into fluorescent products in live cells, while impermeant DNA-binding dyes selectively enter cells with compromised plasma membranes and label nucleic acids in dead or dying cells, enabling discrimination between viable and non-viable populations by fluorescence microscopy or flow cytometry.
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Double or multiplex chromogenic IHC
Double or multiplex chromogenic IHC detects two or more protein targets in the same FFPE tissue section by repeated antigen-antibody binding, enzyme-linked detection, chromogen deposition, image capture, and, for higher-plex workflows, removal or destaining before the next staining cycle. Chromogenic readouts are generated as colored precipitates at antigen sites, enabling evaluation of marker expression, cell phenotype, and spatial relationships in preserved tissue architecture. Classic examples include MICSSS, which performs iterative chromogenic IHC staining, scanning, and destaining on a single slide, and p16/Ki-67 dual staining, which uses chromogenic co-detection to identify cervical cells with combined cell-cycle deregulation and proliferation signals.
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Protein Extraction
Protein extraction uses physical, chemical or biological methods, such as ultrasonic disruption, salting out, cell lysis, electrophoresis, etc., to destroy the cell membrane structure and to separate the proteins from different components according to their characteristics.
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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
純度とドキュメンテーション
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)