ACTH [1-17]

[Description]:

ACTH (1-17), an adrenocorticotropin analogue, is a potent human melanocortin 1 (MC1) receptor agonist with a Ki of 0.21 nM.

[Related Catalog]:

Signaling Pathways >> GPCR/G Protein >> Melanocortin Receptor

Research Areas >> Cancer

Research Areas >> Neurological Disease

Peptides

[Target]

Ki: 0.21 nM (human MC1 receptor)[1]

[In Vitro]

ACTH (1-17) is a potent agonist at the hMC1R. ACTH (1-17) shows high affinity for the hMC1R with a Ki value of 0.21±0.03 nM which is slightly higher than that of 0.13±0.005 nM for alpha-MSH[1]. ACTH (1-17) induces a slight and not significant increase in growth hormone secretion even when micromolar concentrations of the peptide are employed in rat pituitary cultures[2].

[In Vivo]

Inhibition of DNA labeling is noted when the ACTH (1-17) is administered at 2 hr after the beginning of the daily dark span when nocturnal animals become active. When administered at this circadian stage, the larger dose in particular is associated with an inhibition of DNA labeling lasting for 24 hr. The inhibitory effect is much shorter when the same dose is injected 4 hr earlier[3].

[Cell Assay]

Rat pituitary cells are incubated in the presence of varying concentrations of ACTH (1-17) (0.1 nM-1 μM). A significant increase of growth hormone secretion is documented with each concentration[1].

[Animal admin]

Mice[3] The effects of ACTH (1-17) on the rate of DNA labeling in the metaphyseal bone of CD2F1 mice are tested on a chronopharmacological dosing schedule. Groups of mice that has been conditioned to a 12-hr light/12-hr dark schedule are injected at one of six different timepoints, 4 hr apart during ,a single 24-hr span with either a low (0.021 I.U/kg) or a high (20 I.U./kg) dose of ACTH (1-17). Control groups receive injections of a placebo at corresponding timepoints. Subgroups of mice are injected with [3H]thymidine ([3H]Tdr) to follow the changes in DNA labeling in the proximal tibial metaphysis at 15 min and 2, 4, 8, 12 and 24 hr after ACTH (1-17) or placebo treatment[3].

[References]

[1]. Tsatmali M et al. ACTH1-17 is a more potent agonist at the human MC1 receptor than alpha-MSH. Cell Mol Biol (Noisy-le-grand). 1999 Nov;45(7):1029-34.

[2]. Ceda GP, et al. The effects of ACTH (1-17) on GH secretion in vitro. Horm Metab Res. 1987 Aug;19(8):361-3.

[3]. Walker WV, et al. Effect of an adrenocorticotropin analogue, ACTH (1-17), on DNA synthesis in murine metaphyseal bone. Biochem Pharmacol. 1985 Apr 15;34(8):1191-6.

[Related Small Molecules]

Setmelanotide | Bremelanotide Acetate | JNJ-10229570 | MC-4R Agonist 1 | PF-00446687 | SNT-207707 | SNT-207858 | β-MSH (human) trifluoroacetate salt

[ Molecular Formula ]:
C₉₅H₁₄₅N₂₉O₂₃S

[ Molecular Weight ]:
2093.41000

[ Exact Mass ]:
2092.08000

[ PSA ]:
889.75000

[ LogP ]:
3.96140

[ Index of Refraction ]:
1.685

[ Storage condition ]:
-20°C

Click to get detail MSDS

[ Personal Protective Equipment ]:
Eyeshields;Gloves;type N95 (US);type P1 (EN143) respirator filter

[ RIDADR ]:
NONH for all modes of transport

[ WGK Germany ]:
3.0

Differences in cortisol, aldosterone and testosterone responses to ACTH 1-17 administered at two different times of day.

Chronobiologia 14(1) , 39-46, (1987)

The effects of 100 micrograms, i.m. of the analog ACTH 1-17 administered at 0800 and 1800 on the secretion of cortisol, aldosterone and testosterone have been studied in normal subjects: 8 male and 8 ...

Acute and chronic effects of human recombinant GH (hrGH) on adrenal steroidogenesis in children affected with isolated GH deficiency (IGHD).

J. Clin. Endocrinol. Metab. 80(7) , 2251-4, (1995)

In a previous study we demonstrated that, in children affected with isolated GH deficiency, an acute high-dose human recombinant GH (hrGH) treatment increases the 11-deoxycortisol and induces an IGF-I...

N-terminal ACTH fragments increase the CSF beta-EP content in Alzheimer type dementia.

Acta Neurol. Scand 78(2) , 146-51, (1988)

Eleven patients with presenile Alzheimer type dementia (ATD) were treated with N-terminal ACTH fragments for 14 days. No change in cognitive functions was observed during the treatment. A significant ...

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