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Tetracosactide Acetate

CAT#
10-101-01
Synonyms/Alias
Cosyntropin; Tetracosactrin; α1-24-Corticotropin; ACTH(1-24); 1-24-ACTH; 1-24-Corticotropin; ACTH 1-24; ACTH1-24; Cortosyn; Cortrosyn; Tetracosactide; Tetracosapeptide; ACTH (1-24); Tetracosactid; Tetracosactide; Cortrosinta; Actholain; Cortrosyn; Synacthen; Nuvacthen depot; Cortrophin S
CAS No.
16960-16-0
Sequence
H-Ser-Tyr-Ser-Met-Glu-His-Phe-Arg-Trp-Gly-Lys-Pro-Val-Gly-Lys-Lys-Arg-Arg-Pro-Val-Lys-Val-Tyr-Pro-OH acetate salt
M.W/Mr.
2933.5
Molecular Formula
C136H210N40O31S
Source
Synthetic
Long-term Storage Conditions
−20°C
Application
Tetracosactide is used for diagnostic purposes. It is suitable for treatment of adrenal insufficiency of central origin. It can also be used to diagnose Addison's disease.
Description
Tetracosactide is a synthetic peptide, which corresponds to the first 24 amino acids of the naturally occurring hormone ACTH (adrenocorticotropic hormone). It stimulates the adrenal cortex to produce corticosteroids, mineralocorticoids, and, to a lesser extent, androgens.
Areas of Interest
Hormonal therapy

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Tetracosactide Acetate is a synthetic analogue of the naturally-occurring adrenocorticotrophic hormone (ACTH). In the normal situation, ACTH is released from the pituitary gland at the base of the brain. It acts on the adrenal glands to stimulate the production of steroid hormones (glucocorticoids). If the adrenal glands are healthy, a single injection of tetracosactide results in a rise in blood cortisol (hydrocortisone) concentrations in 30 minutes.

Serum cortisol levels remained less than 100 nmol/L in 11 of 13 participants throughout the study. However, two women achieved peak serum cortisol concentrations greater than 400 nmol/L after 10 and 29 weeks of tetracosactide therapy, respectively, allowing withdrawal of corticosteroid replacement. Concurrently, urine glucocorticoid and mineralocorticoid metabolite excretion increased from subnormal to above the median of healthy controls. One of these responders remains well with improving peak serum cortisol (672 nmol/L) 28 months after stopping all treatments. The other responder showed a gradual reduction in serum cortisol and aldosterone over time, and steroid therapy was recommenced after a 28-week period without glucocorticoid replacement.

Gan, E. H., MacArthur, K., Mitchell, A. L., Hughes, B. A., Perros, P., Ball, S. G., ... & Arlt, W. (2014). Residual adrenal function in autoimmune Addison's disease: improvement after tetracosactide (ACTH1–24) treatment. The Journal of Clinical Endocrinology & Metabolism, 99(1), 111-118.

Infantile spasms, which comprise a severe infantile seizure disorder, have a high morbidity and are difficult to treat. Hormonal treatments (adrenocorticotropic hormone and prednisolone) have been the main therapy for decades, although little evidence supports their use. Vigabatrin has been recorded to have a beneficial effect in this disorder. We aimed to compare the effects of vigabatrin with those of prednisolone and tetracosactide in the treatment of infantile spasms.

Lux, A. L., Edwards, S. W., Hancock, E., Johnson, A. L., Kennedy, C. R., Newton, R. W., ... & Osborne, J. P. (2004). The United Kingdom Infantile Spasms Study comparing vigabatrin with prednisolone or tetracosactide at 14 days: a multicentre, randomised controlled trial. The Lancet, 364(9447), 1773-1778.

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