ACTH (11-24) acetate
Based on 1 Customer Validation
ACTH (11-24) (acetate) is an adrenocorticotropic hormone (ACTH) receptor antagonist. ACTH (11-24) is a fragment of adrenocorticotropic and induces cortisol release. ACTH (11-24) can be used for the research of central nervous system.
For research use only. We do not sell to patients.
- Purity : 99.88%
- Formula: C77H134N24O16·xC2HF3O2
- Molecular Weight:1652.04 (free base)
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Storage:
Sealed storage, away from moisture and light, under nitrogen.
Powder -80°C, 2 years , -20°C, 1 year* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light, under nitrogen)
Biological Activity
Description
In Vitro
ACTH (11-24) (acetate) elicits cortisol secretion submaximally in freshly dispersed or cultured beef adrenal cortical cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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Appearance Solid
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Molecular Weight 1652.04 (free base)
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Formula C77H134N24O16·xC2HF3O2
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Color White to off-white
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Synonyms
Adrenocorticotropic Hormone (11-24) acetate
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Sequence
Lys-Pro-Val-Gly-Lys-Lys-Arg-Arg-Pro-Val-Lys-Val-Tyr-Pro
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Sequence Shortening
KPVGKKRRPVKVYP
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Sealed storage, away from moisture and light, under nitrogen
Powder -80°C 2 years -20°C 1 year * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light, under nitrogen)
Solvent & Solubility
In Vitro:
H2O : 50 mg/mL (Need ultrasonic)
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 (270 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
[1]. Li ZG, et al. Adrenocorticotropin(1-10) and -(11-24) promote adrenal steroidogenesis by different mechanisms. Endocrinology. 1989 Aug;125(2):592-6. [Content Brief]
[2]. P F Brain, et al. Acute influences of some ACTH-related peptides of fighting and adrenocortical activity in male laboratory mice. Pharmacol Biochem Behav [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)