Metyrapone

Metyrapone (Su-4885) is a potent and orally active 11β-hydroxylase inhibitor and an autophagy activator, also inhibits the production of aldosterone. Metyrapone inhibits synthesis of endogenous adrenal corticosteroid, decreases glucocorticoid levels, and also affects behavior and emotion. In addition, Metyrapone increases the efficiency of autophagic process via downregulation of mTOR pathway, and interacts with Pseudomonas putida cytochrome P-450. Metyrapone can be used for researching Cushing's syndrome and depression[1][2][3][4][5].

Product Specifications

CAS Number

[54-36-4]

Product Name Alternative

Su-4885

UNSPSC

12352005

Hazard Statement

H302, H315, H319, H335

Target

Autophagy; Cytochrome P450; Endogenous Metabolite

Type

Reference compound

Related Pathways

Autophagy; Metabolic Enzyme/Protease

Applications

Cancer-programmed cell death

Field of Research

Cancer; Endocrinology; Metabolic Disease; Neurological Disease

Assay Protocol

https://www.medchemexpress.com/Metyrapone.html

Purity

99.83

Solubility

DMSO : 100 mg/mL (ultrasonic) |H2O : ≥ 38 mg/mL

Smiles

CC(C1=CC=CN=C1)(C)C(C2=CC=CN=C2)=O

Molecular Formula

C14H14N2O

Molecular Weight

226.27

Precautions

H302, H315, H319, H335

References & Citations

[1]Roozendaal B, et al. Dose-dependent suppression of adrenocortical activity with metyrapone: effects on emotion and memory. Psychoneuroendocrinology. 1996 Nov;21 (8) :681-93.|[2]Jahn H, et al. Metyrapone as additive treatment in major depression: a double-blind and placebo-controlled trial. Arch Gen Psychiatry. 2004 Dec;61 (12) :1235-44.|[3]Daniel E, et al. Effectiveness of Metyrapone in Treating Cushing's Syndrome: A Retrospective Multicenter Study in 195 Patients. J Clin Endocrinol Metab. 2015 Nov;100 (11) :4146-54.|[4]Peterson JA, Ullrich V, Hildebrandt AG. Methyrapone interaction with Pseudomonas putida cytochrome P-405. Arch Biochem Biophys. 1971 Aug;145 (2) :531-42.|[5]Holczer M, et al. A Comprehensive Systems Biological Study of Autophagy-Apoptosis Crosstalk during Endoplasmic Reticulum Stress. Biomed Res Int. 2015;2015:319589.