(S)-Hydroxychloroquine sulfate
(S)-Hydroxychloroquine ((S)-HCQ) sulfate is an isomer of Hydroxychloroquine (HY-W031727). (S)-Hydroxychloroquine sulfate (2.5-20 mg/mL) reduces the rate of insulin degradation in liver homogenates isolated from non-diabetic and diabetic rats. Formulations containing Hydroxychloroquine have been used in the study of malaria, rheumatoid arthritis, and systemic lupus erythematosus.
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- CAS No.: 155204-09-4
- Formula: C18H28ClN3O5S
- Molecular Weight:433.95
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
Description
Chemical Information
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CAS No. 155204-09-4
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Molecular Weight 433.95
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Formula C18H28ClN3O5S
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SMILES
O=S(O)(O)=O.OCCN(CC)CCC[C@H](C)NC1=CC=NC2=C1C=CC(Cl)=C2
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Synonyms
(S)-HCQ sulfate
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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)