1. GPCR/G Protein
    Neuronal Signaling
  2. Melanocortin Receptor
  3. Adrenocorticotropic Hormone (ACTH) (1-39), rat TFA

Adrenocorticotropic Hormone (ACTH) (1-39), rat TFA (Synonyms: ACTH (1-39) (mouse, rat) TFA)

Cat. No.: HY-P1477A Purity: 99.25%
Handling Instructions

Adrenocorticotropic Hormone (ACTH) (1-39), rat (TFA) is a potent melanocortin 2 (MC2) receptor agonist.

For research use only. We do not sell to patients.

Adrenocorticotropic Hormone (ACTH) (1-39), rat TFA Chemical Structure

Adrenocorticotropic Hormone (ACTH) (1-39), rat TFA Chemical Structure

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10 mM * 1 mL in Water USD 9918 In-stock
Estimated Time of Arrival: December 31
500 μg USD 150 In-stock
Estimated Time of Arrival: December 31
1 mg USD 240 In-stock
Estimated Time of Arrival: December 31
5 mg USD 960 In-stock
Estimated Time of Arrival: December 31
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Based on 1 publication(s) in Google Scholar

Other Forms of Adrenocorticotropic Hormone (ACTH) (1-39), rat TFA:

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Adrenocorticotropic Hormone (ACTH) (1-39), rat (TFA) is a potent melanocortin 2 (MC2) receptor agonist.

In Vitro

ACTH 1-39 at concentrations of 100-400 nM has no toxic effect on neurons, while ACTH provides protection from excitotoxic neuronal death induced by glutamate (100 μM), NMDA (1 mM), AMPA (50 μM), and kainate (25 μM). ACTH at 400 nM provides substantial protection in each case. ACTH at either 200 or 400 nM protects neurons from quinolinic acid (25 μM). There is also protection by ACTH from cell death induced by 2 μM H2O2, which gives rise to reactive oxygen species (ROS), with significantly more protection at 400 nM ACTH compared to 200 nM. ACTH gives modest protection against rapid release of nitric oxide (NO) by NOC-12 but not slow release by NOC-18. ACTH (200 or 400 nM) protects neurons from cytotoxic effects of staurosporine (10-20 nM), a classic inducer of cell death via apoptosis. ACTH reduces cell death from 80% to 55%[1].

In Vivo

The icv injection of ACTH significantly reduces cumulative food intake over the observation period compared with the saline/IgG group. The injection of ACTH Ab into the PVN abolishes the anorexigenic effect of ACTH. Infusion icv of ACTH significantly decreases cumulative food intake in rats that receive α-MSH Ab into the PVN and ACTH icv, and food intake is as low as in the group treated with ACTH icv and IgG into the PVN. Injection of either ACTH Ab or α-MSH Ab into the PVN significantly increase cumulative food intake compared with IgG-treated animals; the combined application of both Ab’s do not increase food intake further[2].

Molecular Weight







Room temperature in continental US; may vary elsewhere.

Powder -80°C 2 years
  -20°C 1 year
In solvent -80°C 6 months
  -20°C 1 month
Animal Administration

Male Wistar rats (weight range 225-250 g at purchase) are used throughout the study. Animals receive a PVN application of ACTH Ab (2 μg/rat) or IgG (2 μg/rat); administration of either ACTH (1 nM/rat) or saline icv is performed 5 min later[2].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

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Adrenocorticotropic Hormone (ACTH) (1-39), ratACTH (1-39) (mouse, rat)Melanocortin ReceptorMC ReceptorInhibitorinhibitorinhibit

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