(rel)-Salcolin A
(rel)-Salcolin A is a flavonoid lignan compound with anticancer, anti-inflammatory, and neuroprotective activities. (rel)-Salcolin A has IC50 values ??of 66.69 μM and 56.12 μM against anaplastic thyroid carcinoma cells (HTH83) and papillary thyroid carcinoma cells (TPC1), respectively. (rel)-Salcolin A also inhibits LPS-induced NO production with an IC50 of 14.65 μM. (rel)-Salcolin A exerts its effects by inducing necroptosis in thyroid cancer cells, inhibiting the production of the inflammatory factor NO, and protecting against glutamate-induced neuronal cell damage, with a neuroprotective E50 of 47.44 μM. (rel)-Salcolin A can be used in research related to thyroid cancer, anti-inflammation, and neuroprotection. (rel)-Salcolin A can be naturally extracted from the leaves of Casearia arborea and the stems of Zea mays (corn).
For research use only. We do not sell to patients.
- CAS No.: 1977557-69-9
- Formula: C27H26O11
- Molecular Weight:526.49
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Chemical Information
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CAS No. 1977557-69-9
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Molecular Weight 526.49
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Formula C27H26O11
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SMILES
O=C1C2=C(O)C=C(O)C=C2OC(C3=CC(OC)=C(C(OC)=C3)O[C@H](CO)[C@@H](C4=CC(OC)=C(C=C4)O)O)=C1
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Structure Classification
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Initial Source
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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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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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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
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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
Purity & Documentation
References
[1]. Jung YJ, et al. Lignan and flavonoids from the stems of Zea mays and their anti-inflammatory and neuroprotective activities. Arch Pharm Res. 2015 Feb;38(2):178-85. [Content Brief]
[2]. Santos AL, et al. Exploring the Antiproliferative Activity of Flavolignans From the Leaves of Casearia arborea (Salicaceae). Chem Biodivers. 2025 Dec;22(12):e01489. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)