This study * caught my attention because it examined the pharmacokinetics of GHRP-2 and in so doing compared it to synthetic GH administration.
Basically they found 1mcg/kg of GHRP-2 half as effective as 43mcg/kg of synthetic GH...they found a linear relationship and therefore they conjectured that 2mcg/kg of GHRP-2 would be as effective as 43mcg/kg of synthetic GH.
However the studies participants were prepubescent children of short stature so we should use their weights. Googling revealed that 40lbs would be a decent approximation of such a young undersized male child. That converts to about 18 kilograms.
For synthetic GH that would mean the children received 43mcg * 18kg = 774mcg of GH.
Nutropin reveals that 1 iu of their GH is equal to 333 mcg so that equates to aproximately 2.3iu of GH.
For GHRP-2 that would mean the children received 1mcg * 18kg = 18mcg of GHRP-2.
Using the studies statement that 2mcg/kg of GHRP-2 equalled the synthetic GH dose we arrive at 2mcg * 18kg = 36mcg of GHRP-2 equally 2.3iu of synthetic GH...or further extrapolation 100mcg of GHRP-2 approximately = 6iu of synthetic GH.
I think the above extrapolation is too liberal for adults & thus flawed. So lets be real conservative in our approach and recognize that the studies used saturation doses (1mcg/kg). For adults I would like to stick with the definition of saturation dose of 1mcg/kg... and use that for adults so for a 100kg man that equals 100mcg of GHRP-2. That would mean a single 100mcg dose of GHRP-2 would equal 1.15iu of synthtic GH.
All this approach assumes is that the saturation dose for children produced the equivalent of 1.15iu of synthetic GH therefore the saturation dose for adults will do the same.
So 3 100mcg doses of GHRP-2 per day will conservatively equate to (1.15 x 3) about 3.5iu of synthetic GH. Note that if the average weight of the study children were really 50 pounds then this 3.5iu estimate becomes 4.2ius of synthetic GH.
So it is probably not unrealistic to figure that 100mcg of GHRP-6 dosed three times a day will yield the approximate equivalent of 3.5 to 4 ius of synthetic GH per day in a young adult male.
* Pharmacokinetics and Pharmacodynamics of Growth Hormone-Releasing Peptide-2: A Phase I Study in Children Catherine Pihoker, Gregory L. Kearns, Daniel French and Cyril Y. Bowers, The Journal of Clinical Endocrinology & Metabolism 1998 Vol. 83, No. 4 1168-1172
Abstract
Administration of GH-releasing peptide-2 (GHRP-2) represents a potential mode of therapy for children of short stature with inadequate secretion of GH. Requisite information to determine the dosing route and frequency for GHRP-2 consists of the pharmacokinetics (PK) and pharmacodynamics (PD) for this compound, neither of which have been previously evaluated in children. The purpose of this study was to characterize the PK and PD of GHRP-2 in children with short stature. Ten prepubertal children (nine boys and one girl; 7.7 ± 2.4 yr old) received a single 1 µg/kg iv dose of GHRP-2 over 1 min, followed by repeated (n = 9) blood sampling over 2 h. GHRP-2 and GH were quantitated by specific RIA methods. PK parameters were calculated from curve fitting of GHRP-2 and GH vs. time data. Posttreatment plasma GH concentrations (normalized for pretreatment values) were used as the effect measurement....
Discussion
The pharmacokinetics of GHRP-2 found in our cohort of pediatric patients are similar to those previously reported in healthy adult volunteers after iv administration of the peptide (3). A comparison of the maximum GH response observed after GHRP-2 administration between these two studies revealed similarities in both the magnitude (i.e. mean values = 44 µg/L in children vs. 55 µg/L in adults) and time of maximal response (i.e. average values = 45–60 min for both). The GH responses observed after iv or sc GHRP-2 are also similar to those previously reported after the parenteral administration of GHRP-6, GHRP-1, or GHRH (3, 4, 23, 24).
To our knowledge, our data represent not only the first report of GHRP-2 pharmacokinetics in pediatric patients, but also the first pharmacodynamic assessment of this peptide. Comparison of the serum concentration vs. time profiles for both GHRP-2 and GH in our subjects reveals an equilibration delay in the attainment of peak GH response, a period that we believe corresponds to the time course of GHRP-2 action. This assertion is supported in part by the consistent observation of an equilibration delay between the serum concentrations of GHRP-2 vs. effect (i.e. change GHt) curves, reflected by the production of a counterclockwise hysteresis and our success in using the sigmoid Emax model to effectively determine the pharmacodynamic parameters for GHRP-2. As previously reported by Holdford and Sheiner (22), the successful application of this pharmacodynamic model suggests both linearity and predictability in the drug concentration vs. effect relationship. Given the fact that GH is a proximate biological marker of GHRP (and presumably, GHRP-2) activity (23, 24), our assumptions entailed in the pharmacodynamic analysis of our data appear valid and reflective of the expected pharmacological response of GHRP-2.
Despite the apparent differences in serum GH pharmacokinetics reported after exogenous administration of the hormone (25) as opposed to the administration of GH secretagogues (26, 27, 28, 29, 30), both the pharmacokinetic and pharmacodynamic data from our study can be used to address the potential therapeutic efficacy of GHRP-2 in pediatric patients with GH insufficiency. First, the mean AUC for GH after the iv administration of a single 1 µg/kg dose of GHRP-2 (i.e. 50.7 ng/mL·h) was approximately 50% of the AUC at steady state (i.e. 114.2 ± 32.7 ng/mL·h) previously reported in a study of pediatric patients who received daily sc doses of 43 µg/kg methionyl GH (25). If one assumes linearity in the dose-response relationship for iv GHRP-2, administration of a single 2 µg/kg iv dose would be expected to produce an AUC for GH that would be virtually identical to that observed under steady state conditions after sc administration of the currently recommended daily doses of recombinant human GH (25), doses that have been shown to produce acceptable rates of linear growth in children who are GH deficient (30). Second, both the Cmax (mean, 50.7 ng/mL) and Emax values for GHRP-2 in our patient cohort (mean GH, 67.5 ng/mL) actually exceeded the average Cmax values for GH (37.6 ± 11.6 ng/mL; range, 17.6–49.5 ng/mL) after a single sc dose of 0.1 mg/kg methionyl GH to GH-deficient children (25). Finally, the EC50 for GHRP-2 in our study cohort (1.1 ± 0.6 ng/mL) was substantially less than the Cmax value (7.4 ± 3.8 ng/mL). This particular finding not only supports the adequacy of the 1 µg/kg iv dose of GHRP-2 in producing a desirable biological effect, but also suggests that extravascular administration of this peptide by a route that could be associated with up to a 50% reduction in bioavailability may still produce an acceptable increase in the serum GH concentration sufficient to initiate and sustain a desired growth response. This hypothesis is being tested by our group in dose-ranging studies of oral and intranasal GHRP-2 that are currently underway.
In conclusion, both the pharmacokinetics and pharmacodynamics of iv administered GHRP-2 in short children are predictable and reflective of the potential for therapeutic application of this peptide. The data produced in this investigation will enable the selection of GHRP-2 doses for future evaluation of their bioavailability, safety, tolerance, and efficacy in children.
Lets go!