Salbostatin
Salbostatin is a competitive Trehalase inhibitor, with an IC50 of 8.3 μM against silkworm trehalase and a Ki of 180 nM against porcine trehalase. Salbostatin is isolated from Streptomyces albus. Salbostatin shows no antibacterial activity, and does not inhibit porcine intestinal mucosa sucrase (EC 3.2.1.26) or maltase (EC 3.2.1.20). Salbostatin can be used in studies related to the development of plant protectants.
For research use only. We do not sell to patients.
- CAS No.: 128826-89-1
- Formula: C13H23NO8
- Molecular Weight:321.32
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Endogenous Metabolite Isoforms
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Biological Activity
Description
IC50 & Target
[1]|
Microbial Metabolite |
In Vitro
Salbostatin inhibits silkworm trehalase with an IC50 of 8.3 μM[1].
Salbostatin potently and competitively inhibits porcine kidney trehalase with a Ki = 180 nM, weakly inhibits murine liver aldose reductase, and does not inhibit porcine small intestine saccharase, maltase, or exhibit antibiotic activity[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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CAS No. 128826-89-1
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Molecular Weight 321.32
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Formula C13H23NO8
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SMILES
O[C@H]1[C@H](O)C(CO)=C[C@H](N[C@H]2CO[C@H](CO)[C@@H](O)[C@@H]2O)[C@@H]1O
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Structure Classification
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Initial Source
Streptomyces albus
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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.
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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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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Bacterial live/dead nucleic-acid viability staining
The LIVE/DEAD bacterial viability staining method is based on differential permeability of nucleic-acid-binding fluorescent dyes, most commonly SYTO 9 and propidium iodide (PI), which enables discrimination of bacterial populations with intact versus compromised cytoplasmic membranes. SYTO 9 penetrates both intact and damaged bacterial membranes and binds nucleic acids to produce green fluorescence, whereas propidium iodide penetrates only cells with compromised membranes and fluoresces red while also reducing SYTO 9 signal through competitive binding and fluorescence interactions. The resulting fluorescence pattern is interpreted as a proxy for membrane integrity, which is widely used as an indicator of bacterial viability in microscopy, flow cytometry, and spectroscopic platforms. However, mechanistic studies show that SYTO 9 and PI interactions involve displacement and fluorescence resonance energy transfer effects, which can influence signal interpretation depending on dye ratios a
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)