Inokosterone
Inokosterone is a potential agent target of estrogen receptor 1 in rheumatoid arthritis patients.
For research use only. We do not sell to patients.
- CAS No.: 15130-85-5
- Formula: C27H44O7
- Molecular Weight:480.63
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| Huh-7 | CC50 |
>700 μM
Compound: 12
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Cytotoxicity against human HuH7 cells assessed as reduction in cell viability after 72 hrs by MTS assay
Cytotoxicity against human HuH7 cells assessed as reduction in cell viability after 72 hrs by MTS assay
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[PMID: 26988299] |
| Huh-7 | EC50 |
>100 μM
Compound: 12
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Antiviral activity against Dengue virus 2 DN454009A infected in human HuH7 cells assessed as inhibition of viral RNA level measured 72 hrs post infection by qRT-PCR method
Antiviral activity against Dengue virus 2 DN454009A infected in human HuH7 cells assessed as inhibition of viral RNA level measured 72 hrs post infection by qRT-PCR method
|
[PMID: 26988299] |
Chemical Information
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CAS No. 15130-85-5
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Molecular Weight 480.63
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Formula C27H44O7
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SMILES
CC(CO)CC[C@@H](O)[C@](C)(O)[C@H]1CC[C@@]2(O)C3=CC([C@]4([H])C[C@@H](O)[C@@H](O)C[C@]4(C)[C@@]3([H])CC[C@]12C)=O
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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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Collagen-Induced Arthritis
Collagen-induced arthritis (CIA) is an autoimmune murine model of rheumatoid arthritis in which immunization with type II collagen (CII) emulsified in an adjuvant induces a T cell- and autoantibody-driven inflammatory arthritis characterized by synovial hyperplasia, immune cell infiltration, and joint destruction. The model typically relies on genetically susceptible mouse strains (e. g. , DBA/1) and reproduces key features of human rheumatoid arthritis, including anti-collagen immune responses and progressive joint inflammation. Disease onset generally occurs within ~3-4 weeks after immunization, depending on antigen/adjuvant combinations and protocol variation. The immunopathology is driven by adaptive immune activation against CII, leading to systemic and local joint inflammation mediated by pro-inflammatory cytokines and effector immune cells, making CIA a standard preclinical platform for evaluating immunomodulatory and anti-arthritic interventions.
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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.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)