alpha-Helical CRF (9-41)

Product Namealpha-Helical CRF (9-41)
CAS99658-03-4
MFC22H25IN2O6
MW540.34817
EINECS
MOL File99658-03-4.mol

Chemical Properties

storage temp.	−20°C
form	powder
color	white

Safety Information

WGK Germany	3
Storage Class	11 - Combustible Solids

MSDS

Provider	Language
SigmaAldrich	English

Usage And Synthesis

Uses

α-Helical Corticotropin Releasing Factor (9-41) is a corticotropin releasing factor (CRF) antagonist. α-Helical Corticotropin Releasing Factor (9-41) decreases plasma growth hormone (GH) values in vivo[1][2].

Biochem/physiol Actions

The corticotropin releasing factor (CRF) antagonist α-helical CRF [9-41] exhibits 10-fold higher affinity for rat CRF2α receptors over human CRF2α receptors. It has been used to elucidate the role of CRF in various physiological systems. In colonic epithelium, it abolishes CRF-induced changes in ion secretion, and significantly inhibits CRF-stimulated conductance. It antagonizes the CRF-induced proinflammatory degranulation of perivascular mast cells that are activated in response to acute psychological stress and CRF secretion.

in vivo

α-Helical Corticotropin Releasing Factor (9-41) (10 μg; the third or lateral ventricle of the brain injection; once) significantly decreases plasma GH values^[1]. α-Helical Corticotropin Releasing Factor (9-41) (100 ng/kg; i.c.v. once) affects rhlL-1/β-induced enhancement of the splenic sympathetic activity^[2].

Animal Model:	Adult Sprague-Dawley rats^[1]
Dosage:	10 μg
Administration:	The third or lateral ventricle of the brain injection; 10 μg once
Result:	Abolished the 10 min electroshocks-produced the decreasing of plasma GH levels by injected into the third or lateral ventricle of the brain 45 min before exposure to stress.

Animal Model:	Adult Sprague-Dawley rats with immunity of endogenous somatostatin (SS)^[1]
Dosage:	10 μg
Administration:	Lateral ventricle brain injection; 10 μg once
Result:	Showed no effect on plasma GH values in rats whose endogenous SS had been immunoneutralized, but did interfere with the stimulatory effect of GH-releasing factor (GRF).

Animal Model:	Male Wistar rats with rhlL-1/β injection^[2]
Dosage:	100 ng/kg
Administration:	Intracerebroventricularly injection; 100 ng/kg once
Result:	Completely blocked the rhlL-1/β-induced enhancement of the splenic sympathetic activity, but failed to alter the enhancement of nociceptive behaviors caused by rhlL-1/β.

References

[1] Rivier C, Vale W. Involvement of corticotropin-releasing factor and somatostatin in stress-induced inhibition of growth hormone secretion in the rat. Endocrinology. 1985 Dec;117(6):2478-82. DOI:10.1210/endo-117-6-2478
[2] Takakazu Oka, et al. Intracerebroventricular injection of interleukin-1/β induces hyperalgesia in rats. Brain Research, 624 (1993) 61-68.

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