BIO-11006
Based on 1 publication(s) in Google Scholar
BIO-11006 is a peptide that inhibits the function of the MARCKS protein. BIO-11006 attenuates LPS-induced neutrophil influx into the lungs, NF-κB activation, and expression of the proinflammatory cytokines KC and TNF-α. BIO-11006 also reverses disease progression in an LPS-induced mouse lung injury model. BIO-11006 is indicated for research on acute lung injury/acute respiratory distress syndrome (ALI/ARDS).
For research use only. We do not sell to patients.
- CAS No.: 901117-03-1
- Formula: C46H75N13O15
- Molecular Weight:1050.17
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) BIO-11006
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Biological Activity
Description
Chemical Information
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CAS No. 901117-03-1
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Molecular Weight 1050.17
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Formula C46H75N13O15
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SMILES
CC(NCC(N[C@@H](C)C(N[C@@H](CCC(N)=O)C(N[C@H](C(N[C@@H](CO)C(N[C@@H](CCCCN)C(N[C@@H]([C@H](O)C)C(N[C@@H](C)C(N[C@@H](C)C(N[C@H](C(O)=O)CCCCN)=O)=O)=O)=O)=O)=O)CC1=CC=CC=C1)=O)=O)=O)=O
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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.
Publications (1)
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Journal Impact Factor
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Most Recent
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Mol Biol Rep
MARCKS N-terminal sequence-derived inhibitor peptides impair monocytic ROS production and migration via MARCKS-independent effects. [Abstract]2025 Sep 17;52(1):911. PMID: 40960646
Protocols
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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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
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Inhalation Toxicity Study
Inhalation toxicity studies expose rodents to a controlled aerosol, vapor, gas, or smoke atmosphere and assess respiratory and systemic toxicity using exposure-atmosphere characterization, clinical observations, body and organ weights, bronchoalveolar lavage fluid, histopathology, blood chemistry, hematology, and, when included, molecular endpoints such as transcriptomics, proteomics, lipidomics, or tissue burden analysis. The primary biological readouts are airway irritation, pulmonary inflammation, cytotoxicity, altered surfactant or lipid homeostasis, impaired particle clearance, and tissue remodeling, reflected by BALF cell differentials, BALF protein, LDH, phosphatase activities, cytokines, lung weight, microscopic respiratory-tract lesions, and retained lung burden.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)