Hexarelin 2mg & CJC-1295 DAC 2mg Bundle Properties

Hexarelin 2mg

Chemical Formula: C47H58N12O6
Molecular Weight: 887.1g/mol
Synonyms: Hexarelin, Examorelin, L-Lysinamide
CAS Number: 140703-51-1
PubChem: 6918297
Total Amount of the Active Ingredient: 2mg (1 vial)
Shelf Life: 36 months

CJC-1295 DAC 2mg

Chemical Formula: C152H252N44O42
Molecular Mass: 3647.28
Synonyms: CJC1295 Without DAC, CJC1295 With DAC, 446262-90-4
Molar Mass: 3367.9
CAS Number: 446036-97-1
PubChem: 91976842
Total Amount of the Active Ingredient: 2mg (1 vial)
Shelf Life: 36 months

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Peer-Reviewed Studies

Hexarelin modulates lung mechanics, inflammation, and fibrosis in acute lung injury

Abstract

Introduction: Acute respiratory distress syndrome (ARDS) is an acute form of diffuse lung injury characterized by (i) an intense inflammatory response, (ii) increased pulmonary vascular permeability, and (iii) the loss of respiratory pulmonary tissue. In this article we explore the therapeutic potential of hexarelin, a synthetic hexapeptide growth hormone secretagogue (GHS), in an experimental model of ARDS. Hexarelin has anti-inflammatory properties and demonstrates cardiovascular-protective activities including the inhibition of cardiomyocyte apoptosis and cardiac fibrosis, both of which may involve the angiotensin-converting enzyme (ACE) system.

Methods: In our experimental model, ARDS was induced by the instillation of 100 mM HCl into the right bronchus; these mice were treated with hexarelin (320 μg/kg, ip) before (Pre) or after (Post) HCl challenge, or with vehicle. Respiratory system compliance, blood gas analysis, and differential cell counts in a selective bronchoalveolar lavage (BAL) were determined 6 or 24 hours after HCl instillation. In an extended study, mice were observed for a subsequent 14 days in order to assess lung fibrosis.

Results: Hexarelin induced a significant improvement in lung compliance and a reduction of the number of total immune cells in BAL 24 hours after HCl instillation, accompanied with a lower recruitment of neutrophils compared with the vehicle group. At day 14, hexarelin-treated mice presented with less pulmonary collagen deposition compared with vehicle-treated controls.

Conclusions: Our data suggest that hexarelin can inhibit the early phase of the inflammatory response in a murine model of HCl-induced ARDS, thereby blunting lung remodeling processes and fibrotic development.

Growth hormone status during long-term hexarelin therapy

Hexarelin, a powerful GH-releasing peptide, is capable of causing profound GH release in normal subjects after oral, intranasal, iv, and sc administration. The effect of long-term administration on GH levels in adults is unknown. We have, therefore, assessed the effects of 16 weeks of twice-daily sc hexarelin therapy (1.5 μg/kg BW) on the GH response to a single injection of hexarelin, and also the GH response to hexarelin 4 weeks after cessation of hexarelin therapy. We have also assessed the effects of chronic hexarelin therapy on serum insulin-like growth factor (IGF)-I, IGF binding protein-3, markers of bone formation (osteocalcin, procollagen-type-III-N-terminal-peptide, and C-terminal propeptide of type I collagen), and resorption (urinary deoxypyridinoline and pyridinoline), body composition, and bone mineral density.

The mean (±sem) area under the GH curve (AUC_GH) at weeks 0, 1, 4, 16, and 20 were 19.1 ± 2.4μ g/L·h, 13.1 ± 2.3 μg/L·h, 12.3 ± 2.4 μg/L·h, 10.5 ± 1.8 μg/L·h, and 19.4 ± 3.7 μg/L·h, respectively. There was a significant change in AUC_GH over the study period (P = 0.0003). Further analysis showed that, compared with baseline, the decrease in AUC_GH at week 4 and week 16 were significant (P < 0.05 and P < 0.01, respectively). Four weeks after completion of hexarelin therapy, the AUC_GH increased significantly, compared with AUC_GH at week 16 (P < 0.05), and was not significantly different from that at week 0.

Serum IGF-I and IGF binding protein-3 did not change significantly over the 20-week period (P = 0.24 and P = 0.74, respectively). Of the bone markers measured, only serum C-terminal propeptide of type I collagen changed significantly and was higher at week 16, compared with baseline (P = 0.019). Total body fat, lean body mass, and bone mineral density had not changed significantly at week 16, compared with baseline (P = 0.6, P = 0.3, and P = 0.3, respectively).

In summary, we have demonstrated that chronic hexarelin therapy results in a partial and reversible attenuation of the GH response to hexarelin. In the present study, the biological impact of this hexarelin schedule on the GH-IGF-I axis seems to be minimal. The therapeutic potential of chronic hexarelin requires further investigation.

Cardiac effects of hexarelin in hypopituitary adults

Abstract

Growth hormone (GH)-releasing peptides possess specific pituitary, hypothalamic, and myocardial receptors. Seven adult male patients with GH deficiency (GHD) (age, mean±S.E.M.: 42.0±4.0 year) were studied by equilibrium radionuclide angiocardiography after i.v. administration of hexarelin, a peptide GH secretagogue. Data for these patients were compared with those for nine adult male controls (37.0±2.7 year). The GH response to hexarelin was negligible in patients with GHD compared to control subjects (CS) (peak: 1.9±0.9 vs. 45.7±3.6 μg/l, P<0.001). Basal left ventricular ejection fraction (LVEF) in patients with GHD was lower than that in CS (50±1% vs. 63±2%, P<0.001). Hexarelin administration increased LVEF both in patients with GHD and in CS (peak: 57±2 vs. 70±2, respectively, P<0.05 vs. baseline) without changing catecholamine levels, mean blood pressure (MBP), or cardiac output in either group. In conclusion, the acute administration of hexarelin exerts a short-lasting positive inotropic effect in humans, probably GH-independent and mediated by specific myocardial receptors for GH secretagogues.

Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults

Abstract
Context: Therapeutic use of GHRH to enhance GH secretion is limited by its short duration of action.

Once-daily administration of CJC-1295, a long-acting growth hormone-releasing hormone (GHRH) analog, normalizes growth in the GHRH knockout mouse

Abstract
Although the majority of children with isolated growth hormone (GH) deficiency have a good growth response to GH-releasing hormone (GHRH), the use of this therapeutic agent is limited by its very short half-life. Indeed, we have shown that, in mice with GHRH gene ablation (GHRH knockout; GHRHKO), even twice-daily injections of a GHRH analog are unable to normalize growth. CJC-1295 is a synthetic GHRH analog that selectively and covalently binds to endogenous albumin after injection, thereby extending its half-life and duration of action. We report the effects of CJC-1295 administration in GHRHKO animals. Three groups of 1-wk-old GHRHKO mice were treated for 5 wk with 2 μg of CJC-1295 at intervals of 24, 48, and 72 h. Placebo-treated GHRHKO mice and mice heterozygous for the GHRHKO allele served as controls. GHRHKO animals receiving daily doses of CJC-1295 exhibited normal body weight and length. Mice treated every 48 and 72 h reached higher body weight and length than placebo-treated animals, without full growth normalization. Femur and tibia length remained normal in animals treated every 24 and 48 h. Relative lean mass and subcutaneous fat mass were normal in all treated groups. CJC-1295 caused an increase in total pituitary RNA and GH mRNA, suggesting that proliferation of somatotroph cells had occurred, as confirmed by immunohistochemistry images. These findings demonstrate that treatment with once-daily administration of CJC-1295 is able to maintain normal body composition and growth in GHRHKO mice. The same dose is less effective when administered every 48 or 72 h.

Netnography of Female Use of the Synthetic Growth Hormone CJC-1295: Pulses and Potions

Abstract
Background: Communal online folk pharmacology fuels the drive for short cuts in attaining muscle enhancement, fat loss, and youthful skin.

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The information provided above is not intended to substitute medical advice, diagnosis, or treatment. Should you have any questions regarding a medical condition, seek the advice of your physician or a qualified healthcare provider. In no case should medical advice be disregarded or delayed because of what you have read or seen. We bear no responsibility or liability for your use of any of our research compounds and products. Please note that they are being sold for research purposes ONLY. We do NOT condone any personal use.

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ALL ARTICLES AND PRODUCT INFORMATION PROVIDED ON THIS WEBSITE ARE FOR INFORMATIONAL AND EDUCATIONAL PURPOSES ONLY.

The products offered on this website are furnished for in-vitro studies only. In-vitro studies (Latin: “in glass”) are performed outside the body. These products are not medicines or drugs and have not been approved by the FDA to prevent, treat and/or cure any medical condition, ailment or disease. Bodily introduction of any kind into animals or human is strictly prohibited by law.