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Old 10-30-2006, 08:19 PM
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TCS
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GHRH, sermorelin , CJC-1295 or HEXARELIN?

Sermorelin acetate is the acetate salt of an amidated synthetic 29–amino acid peptide (GRF 1-29 NH 2) that corresponds to the amino-terminal segment of the naturally occurring human growth hormone–releasing hormone (GHRH or GRF) that consists of 44 amino acid residues.

sermorelin acetate ( 1-29 )

H-Tyr-Ala-Asp-ALa-lle
-Phe-Thr-Ser-Ser-Tyr-Arg-Lys
-Val-Leu-Gly-Gln-Leu-Ser-Ala
-Arg-Lys-Leu-Leu-Gln-Asp-lle
-Met-Ser-Arg-NH2

regular GHRH (1-44 )

H-Tyr-Ala-Asp-ALa-lle
-Phe-Thr-Ser-Ser-Tyr-Arg-Lys
-Val-Leu-Gly-Gln-Leu-Ser-Ala
-Arg-Lys-Leu-Leu-Gln-Asp-lle
-Met-Ser-Arg-Gln-Gln-Gly-Glu
-Ser-Asn-Gln-Glu-Arg-Gly-Ala
-Arg-Ala-Leu-NH2

Like naturally occurring GHRH, sermorelin stimulates the pituitary gland to release growth hormone, resulting in an increase in the concentration of growth hormone in the plasma.

There is also CJC-1295 which amino acid sequence consists of the same 29 amino acids from sermorelin acetate except there are 4 substitutions on positions 2, 8, 15 and 27.

1 H-Tyr-(D) Ala-Asp-Ala-Ile
-Phe-Thr-Gln-Ser-Tyr-Arg-Lys
-Val-Leu-Ala-Gln-Leu-Ser-Ala
-Arg-Lys-Leu-Leu-Gln-Asp-Ile
-Leu-Ser-Arg-NH2

CJC-1295 of course is the final outcome of this modified peptide which extends its life considerably, however some may be hesitant to try CJC-1295 due to the death report on one of the testers who was an AIDS patient on a recent clinical trial it has been reported his death had nothing to do with CJC-1295 administration.

Sermorelin acetate can be used at least 1mg daily before retiring to stimulate GH release for at least a month.

For those seeking for an alternative to illegal GH this novel peptide ( sermorelin acetate or CJC-1295 ) can help elevate natural endogenous levels.

GHRP-6 is also good at doing this but there are some studies showing Hexarelin has a greater GH releasing activity than GHRH, my question is ..does this mean greater than of sermorelin acetate or CJC-1295?

Growth hormone-releasing activity of hexarelin, a new synthetic hexapeptide, after intravenous, subcutaneous, intranasal, and oral administration in man
E Ghigo, E Arvat, L Gianotti, BP Imbimbo, V Lenaerts, R Deghenghi and F Camanni
Department of Clinical Pathophysiology, University of Turin, Italy.



We evaluated the GH-releasing activity of hexarelin, a new synthetic hexapeptide, after i.v. (1 and 2 micrograms/kg), sc (1.5 and 3 micrograms/kg), intranasal (20 micrograms/kg), and oral (po; 20 and 40 mg) administration to 12 healthy young volunteers. Reference treatments were i.v. saline and GH-releasing hormone (GHRH; 1 microgram/kg). GH release (mean +/- SEM) after the i.v. dose of 1 microgram/kg hexarelin [area under the curve (AUC), 3175 +/- 506 micrograms/min.L] was about 2 times higher than that induced by 1 microgram/kg GHRH (AUC, 1544 +/- 161 micrograms/min.L; P < 0.001). Hexarelin (2 micrograms/kg, i.v.) elicited a further increase in GH levels (AUC, 4422 +/- 626 micrograms/min.L) compared to the 1 microgram/kg dose. The GH response to 2 micrograms/kg hexarelin, i.v., was very reproducible (AUC, 4016 +/- 563 vs. 3959 +/- 803 micrograms/min.L). The sc administration of hexarelin produced a dose-dependent GH response (AUC, 3180 +/- 392 and 4459 +/- 566 micrograms.min.L with 1.5 and 3 micrograms/kg, respectively). Intranasal administration of 20 micrograms/kg hexarelin induced GH release (AUC, 2642 +/- 452 micrograms/min.L) similar to that caused by 1 microgram/kg, i.v. Twenty and 40 mg hexarelin, po, produced a dose-related increase in GH levels (AUC, 2278 +/- 442 and 4079 +/- 514 micrograms/min.L). Biological bioavailabilities were 77.0 +/- 10.5%, 4.8 +/- 0.9%, and 0.3 +/- 0.1% for the sc, intranasal, and po routes, respectively. This study shows that the GH response to hexarelin administered by the i.v. route has a limited variability and is superior to the response to GHRH. The GH-releasing activity appeared to be dose dependent. Thus, hexarelin could be clinically useful to stimulate GH secretion in humans.

Hexarelin is a stronger GH-releasing peptide than GHRH in normal cycling women but not in anorexia nervosa.

Giusti M, Foppiani L, Ponzani P, Cuttica CM, Falivene MR, Valenti S.

DISEM, Cattedra di Endocrinologia, University of Genova, Italy.


Anorexia nervosa (AN) is a chronic disease in which an enhanced GH response to GHRH, a paradoxic increase after TRH and LHRH, and low IGF1 levels may be present according to the patient's clinical state. It is well known that the GH hypersecretory state commonly found in the "acute phase" of AN is restored with weight gain. The new synthetic hexapeptide, Hexarelin (HEX), which is chemically similar to GH-releasing peptide 6, has recently been shown to possess a stronger GH-releasing activity than GHRH in humans and to share a synergistic effect with GHRH when administered intravenously. Indeed, HEX shows a slight cortisol and PRL-releasing activity. The aim of the study was to evaluate the effect of i.v. administration of old (GHRH) and new (HEX) GH-releasing peptides on GH, PRL and cortisol secretion in 9 AN patients in the "recovery phase" of the disease, after partial but significant weight gain. For controls we studied 7 normal cycling women. No significant difference in GH secretion after GHRH was found between AN and controls. GHRH was not able to release cortisol or PRL either in AN or controls. HEX produced a significantly (p < 0.05) higher GH peak in controls than in AN, while GH AUC was slightly but not significantly higher. Indeed, only in controls, HEX was a stronger GH-releasing peptide than GHRH. These findings could be explained by the fact that, in AN, GH secretion is already stimulated both by reduced IGF1 levels and by increased GHRH/somatostatin ratio. As reported in the literature, the action of HEX action is only slightly influenced by variations in somatostatin tone. It therefore appears likely that the absolute or relative GHRH increase present in AN could partially mimic the unknown hypothalamic factor necessary for HEX action on the hypophisis and that, following a structural modification of pituitary HEX receptors, GHRH would become able to bind to HEX receptors on somatotropic cells. Consequently, the pituitary cells would already be over-activated and so unable to respond maximally to HEX stimulation. Indeed, in AN, GHRH might play a role of negative modulation in the control of HEX action. Finally, in our study HEX was able to produce a persistent PRL release in controls but not in AN, thus suggesting that its action could be partially dependent on the estrogen milieu, while it stimulated cortisol secretion only transiently in the patients studied.

Publication Types:
Clinical Trial
Randomized Controlled Trial

PMID: 9258804 [PubMed - indexed for MEDLINE]

Here is a link with full detailed info on CJC-1295: http://jcem.endojournals.org/cgi/con...jc.2005-1536v1

Which do you think is best?

Thanks,

C
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