KS IV
KS IV is a cyclolignan derivative and antigonadotropic agent. KS IV exhibits activity against pregnant mare serum gonadotropin (PMSG) but shows no activity against luteinizing hormone (LH). KS IV abolishes the stimulatory effect of PMSG on testosterone release from isolated mouse Leydig cells. KS IV can be used in studies on gonadotropin-regulated endocrine functions.
For research use only. We do not sell to patients.
- CAS No.: 121242-02-2
- Formula: C17H12O6
- Molecular Weight:312.27
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Storage:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
In Vitro
KS IV (compound 2) (0.09-0.9 μg) completely inhibits testosterone release from isolated mouse Leydig cells induced by 0.05 IU PMSG (HY-N12634)[1].
KS IV (0.09-0.9 μg) shows no activity against testosterone release induced by 25 ng LH (HY-P2293) in isolated mouse Leydig cells[1].
The relative molecular mass of KS IV determined by negative-ion FAB mass spectrometry is 312[1].
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. 121242-02-2
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Appearance Solid
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Molecular Weight 312.27
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Formula C17H12O6
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Color White to off-white
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SMILES
OC1=CC=C(C=C1O)C2=C3C=C(C(O)=CC3=CC(C(O)=O)=C2)O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
Protocols
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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
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Data Sheet (284 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
KS IV Related Classifications
HY-117671 Related Classifications
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