Dat's - CJC-1295 & GHRP-6 (Basic Guides)

xxxxx said:

My question still is whether or not using MGF in a stand alone fashion is sufficient enough to elicit new cellular growth that can then be enacted upon by AAS to mature newly produced cells.

...wondering if using one of the end products that seems to be majorly responsible for cellular reproduction/proliferation would be appropriate/sensible to use alone.

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You need MGF & IGF-1.

Where are you going to get your IGF-1 from? More importantly where are you going to get your IGF-1 localized in muscle from?

DatBtrue said:

I am fumbling forward on this as well.

I believe that MGF will be beneficial. What I am not clear on is IF non-peg MGF can be used effectively. The problem as you know is that it degrades quickly and has a tiny effective target area, while peg-MGF is resistant to plasma degradation and has a wider effective target area.

With MGF we don't want it to circulate in the blood stream. We want it to be immediately taken up in the muscle we inject into. So I was thinking regular MGF might be effective if it is injected in multiple location in the target muscle in a way that is similar to the way you would inject/use site enhancing oil.. then also administer it more frequently then you would peg.



CJC-1295 will elevate IGF-1 levels but GHRP-6/GHRP-2/Hexarelin will not do so on a continual basis.

Actually both of these questions get into the following.

There are two "categories" of GH as well as two "categories" of IGF-1.

One is systemic, the other autocrine/paracrine (locally made/used).

The systemic is either secreted by the pituitary and released into circulation for growth hormone or synthesized in the liver and released into the bloodstream for IGF-1.

Of course injected forms of GH & IGF-1 are systemic...but what is this about local effects we hope for?

The local effect has to be distinguished from the second category autocrine/paracrine.

This second category is made up of GH or IGF-1 that is created in local non-liver tissue (in our case muscle) and used in that same location.

This second category autocrine/paracrine (locally made/used) is more important then the first category as it pertains to growth and especially IGF-1.

So we spend so much time thinking about general circulating IGF-1 levels we fail to consider that it isn't nearly as important as IGF-1 made in the muscle or as I call it muscle IGF-1.

The physiological role (or effective importance) of autocrine/paracrine GH is to provide local tissue needs for GH above that supplied by pituitary-derived GH or to provide GH in compartments/areas where GH has no ready access.

But with specific regard to IGF-1 it has been demonstrated that muscle IGF-1 is more important then circulating liver synthesized IGF-1 in promoting growth.

Here is how autocrine/paracrine production appears to occur. If you understand this then you can see why local injections may not have the same effect.

Paracrine GH is produced inside the muscle cell and binds to the the GH receptor immediately after synthesis in the endoplasmic reticulum of he cell. This binding facilitates maturation of GH receptor and creates a self-bound complex which then makes its way to the cell surface. The signalling is yet to be turned on inside the cell and it is not until the complex moves to the cell surface that signalling begins.

As you can see GH that comes into the area from general circulation will not have a chance to bind to this growth hormone receptor because it was birthed in an already bound state. *

There is some evidence that the same thing happens with IGF-1 autocrine/paracrine action in muscle BUT there is also evidence that there are still unbound receptors available as well. **

So this is the sort of thing that I continue to puzzle over.

I will post some interesting material that I had previously posted at AM on MGF.

References:

* Autocrine Growth Hormone: Effects on Growth Hormone Receptor Trafficking and Signaling, Monique J. van den Eijnden and Ger J. Strous, Molecular Endocrinology 2007 21 (11): 2832-2846

** Interaction of Secreted Insulin-like Growth Factor-(II GF-I) with Cell Surface Receptors Is the Dominant Mechanism of IGF-1’s Autocrine Actions, Zonghan Dai, Alan D. Stiles, Billie Moats-Staats, JudsoJn. Van Wyk, and A. Joseph D’Ercole, Journal of Biol Chem Vol. 267, No. 27, Issue of September 25, pp. 19565-19571,1992​

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I fully understand what your saying. You say there is evidence of unbound receptors for IGF. Wouldn't that definitely be true, because systemic release of GH, then causing systemic release of IGF from the liver, does indeed have affects on muscle as a given. I read in a book (Ironman i think) that increases in testosterone has an affect on lowering igf receptors in a muscle.. BUT that also testosterone increases systemic, and autocrine/paracrine levels of IGF. (Nice little check and balance there it seems)
Nandrolone increases production of IGF, and also reduces levels of binding proteins that inhibit IGF, and that Trenbolone increases muscle fiber sensitivity to IGF.
(I didn't know that receptor sites could be decreased or increased - confused on that)

It is a little puzzling to me also on whether cycling IGF and mgf is worth it with the GHRP/CJC.

Another question for you:
If Insulin stops GH secretions temporarily, would that mean timing should be paid more attention to as far as conjunction cycling of GH releasing peptides like CJC and GHRP, and insulin?

Thanks for taking the time to reply to me DAT

DatBtrue said:

You need MGF & IGF-1.

Where are you going to get your IGF-1 from? More importantly where are you going to get your IGF-1 localized in muscle from?

View attachment 21776

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Hello Dat, what do you think of Sermorelin? Please give some comments. Thanx!

AK.Lab said:

Hello Dat, what do you think of Sermorelin? Please give some comments. Thanx!

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Sermorelin = Growth Hormone Releasing Hormone (GHRH)

GHRH ( hGHRH-(1-44)-NH2 ) is a 44 amino acid chain. The biologically active portion was found to reside in the first 29 amino aids.

So those unneeded amino acids were removed to form a 29 amino acid chain GHRH-(1–29)-NH2.

The common nomenclature for this biologically active 29 amino acids is now GRF-(1-29).

"Synthetically produced GRF (Sermorelin) has an amino acid composition identical to the N-terminal 29 amino acids 1–29 sequence of the natural hypothalamic GHRH. It maintains bioactivity in vitro and is almost equally effective in eliciting secretion of endogenous growth hormone in vivo. The main drawbacks associated with the pharmaceutical use of hGRF relate to its short half-life in plasma, about 10–20 min in human." - PEGylation of growth hormone-releasing hormone (GRF) analogues, P. Esposito et al., Advanced Drug Delivery Reviews 55 (2003) 1279–1291


So Sermorelin is the drug name for an FDA approved synthetic of GHRH. The primary drawback is that it is subject to enzymatic degradation. Within the first 10 minutes the first 3 amino acids are cleaved off in plasma rendering it ineffective to promote further growth hormone release.

Thus frequent injections of Sermorelin are needed.

To overcome this limitation many types of analogs were created to extend the half-life.

One early analog was created via a simple amino acid substitution to produce D-Ala2-GHRH-(1-29). The D-Ala2 analog was found to enjoy a reduced metabolic clearance and enhanced binding affinity. Together these factors contributed to a 2-fold increase in GH-releasing activity in humans. (NOTE: it was found to be 50 times more potent in rats so sometimes someone claims it to be 50 times more potent....but in humans it is only twice as potent).

Another amino acid substituted analog (Nle27)-GHRH-(1-29)-NH2 was found to have biological activity for two hours. In a study where 10mcg/kg were given pre-bed to older subjects they found positive benefits attributed to high GH levels over the course of many months. - Endocrine and Metabolic Effects of Long-Term Administration of [Nle27]Growth Hormone-Releasing Hormone-(1-29)-NH2 in Age-Advanced Men and Women J, O. Khorram, Clin. Endocrinol. Metab., May 1997; 82: 1472 - 1479

Besides amino acid substitution other methods have been used such as PEGylation. It is possible to create longer lasting analogs of GHRH and the literature is full of effective example. See Generally: Synthesis and Biological Evaluation of Superactive Agonists of Growth Hormone-Releasing Hormone, J Izdebski, J Pinski, JE Horvath, G Halmos, K Groot and AV Schally, Proceedings of the National Academy of Sciences, Vol 92, 4872-4876

However the most effective GHRH analogs with the longest half-life are those that were created with an attached complex (3-maleimidopropionic acid (MPA) unit) which enables them to attach to albumin once injected into blood plasma. This binding to albumin not only increased the half life but helped to stabilize the active peptide portion from degradation by plasma enzymes. This bioconjucation method was used to create the GHRH analogs CJC-1293 & CJC-1295.

The early research studied three analogs. They were:

CJC-1288 an hGRF1-29 with an extra lysine (Lys) at the 30-position to accommodate a 3-maleimidopropionic acid (MPA) unit; and

CJC-1293 which is equivalent to CJC-1288 but with a D-alanine (D-Ala) at the 2-position; and

CJC-1295 which is a tetrasubstituted analog of CJC-1288 but with a D-Ala at the 2-position, a glutamine (Gln) at the 8-position, an Ala at the 15-position, and a leucine (Leu) at the 27-position.

CJC-1295 emerged as the construct of choice based on the absolute amount of GH secreted in test rats over a two hour period amounting to twice that of the next best compound CJC-1293.

While CJC-1295 was chosen for testing on human subjects I think it is worth noting that to my layman's eyes it may not be considered vastly superior to CJC-1293 for the following reasons.

In Vitro stability tests indicated that the amount of compound remaining (i.e. non-degraded) after a 24 hour period was 90% for CJC-1295 but 99% for CJC-1293.

The In Vivo test that resulted in CJC-1295's superiority in absolute GH secreted over 120 minutes never-the-less revealed that CJC-1293 had thrice (3x) the amount of GH release at the 120 minute mark than CJC-1295. CJC-1293 exhibited a /\/ shaped curve with a medium trough while CJC-1295 exhibited more of a rise and fall /\ shaped curve.

The primary reason for pointing out CJC-1293's effectiveness is that it may come to pass that CJC-1295 may become unavailable perhaps because no chemical lab will synthesize it in violation of the patent (if it becomes a drug), leaving other less protected or yet to be created structures available for laboratory synthesis by private order.

So in summary Sermorelin is the drug name for Growth Hormone Releasing Hormone (GHRH). It has very little therapeutic value and is primarily used as a diagnostic tool. Longer acting analogs of GHRH have been studied and have been found to be of therapeutic value. The most successfull such analog to date that has been tested in humans is CJC-1295. Its long half-life is attributed to its Drug Affinity Complex (DAC) which enables it to bind to albumin in plasma & thus resist degradation.

Dat-

very new here but WOW! this thread is impressive!!!!!


so there is just so much in here its hard to understand a lot! you are like a mad scientist haha.

mucho respecto

Smooth

DatBtrue said:

CJC-1293 exhibited a /\/ shaped curve with a medium trough while CJC-1295 exhibited more of a rise and fall /\ shaped curve.

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To start on a new note.

Which curve shape would be better for the preservation of the natural pulsation of GH?

likkayouth said:

To start on a new note.

Which curve shape would be better for the preservation of the natural pulsation of GH?

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Pulsation would probably be preserved under either as was demonstrated in the pulsation study for CJC-1295.

Its almost like GHRH (CJC-12xx as its analog) doesn't impose an unnatural will on receptor level signaling whereas synthetic GH does.

I believe that is why Massive G and then other bodybuilders discovered that results with synthetic GH were better if dosed EOD (or at least with breaks).

likkayouth you have a bright active mind. I don't mind interacting with you in the least. I'm glad you didn't disappear because I wasn't willing to get into the question you raised at AM.

DatBtrue said:

likkayouth you have a bright active mind. I don't mind interacting with you in the least. I'm glad you didn't disappear because I wasn't willing to get into the question you raised at AM.

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Thank you.
There is no way I'll disappear. I find all this information and research field fascinating, and your contribution to the explanation of it all is extraordinary. I wish everyone would support their own statements with research documents like that ...

I started my own niche of research on the topic. This weeks it's been 2x200mcg GHRP-6, an afternoon and a pre-bed dose, because that's how much finances I have right now
Next week I'll add 50mcg CJC-1295 to the mix, with a dose of arginine right before each injection, just in case.

For the past 2 days the research subject has faster than usual recovery between sets of whatever exercise, and seems to be fresh after strenuous training sessions. Permanent need for food seems to be at hand as well.

Eventually I'd like to add MGF, and will probably opt out for the pegylated version, only because it will remain stable for a longer period after reconstitution. If that wasn't an issue, the regular MGF would've been my choice.

I was wondering what effect pGH would have on the CJC-1295+GHRP-6 combination. In your post #77 on AM you said:

DatBtrue said:

You could use the pGH before bed w/ CJC. I wouldn't drop the GHRP-6 but just use a little dose. One study found that using just 30mcg of GHRP-2 w/ GHRH greatly amplified the pulse. So you could use CJC + a little bit of GHRP-6 + pGH.

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However I don't think you have explained what the contribution of pGH would be. And I am very curious to know, since it is relatively inexpensive. Also, how about gaba powder?

And as last question, since the effect of high levels of GH is synergistically amplified by high levels of testosterone, do you know of legal OTC substances/methods that increase the levels of endogenous testosterone, even if not dramatically?

likkayouth said:

I was wondering what effect pGH would have on the CJC-1295+GHRP-6 combination. In your post #77 on AM you said:
...
However I don't think you have explained what the contribution of pGH would be. And I am very curious to know, since it is relatively inexpensive. Also, how about gaba powder?

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Night-time GH release and "Slow Wave Sleep" seem to be two sides of the same coin. Increase/decrease one and the other increases/decreases as well. The full post was as follows:

Q: Anyway Dat, do you think that tyric-6 could be utilized with CJC and produce results comparable to a once a day administration of CJC/GHRP-6?

Dat: Comparable results? Hell no!

Q: Maybe CJC/GHRP-6/tyric-6? Seems that GHRP-6 would be ideal, but my research subject has alot of PGH..

Dat: I'm in a position to answer the question because I started with just pGH for about three months. My sleep was awesome and after three months I KNEW that my growth hormone levels had a subtle bump up thanks to gaba/gabob. I just looked in the mirror and realized I felt a lot better. Someone once guesstimated that it gave a 1iu GH equivalent boost.

Then I ran GHRP-6 by itself for a couple of months and I felt that my body had a much larger bump in GH levels as a result...more along the lines of a 3iu GH equivalent. These numbers don't mean anything by-the-way I am just using them for a relative comparison. [3 to 1... 4 to 1]

I took a one week break from GHRP-6 and just used the pGH. I felt subjectively that it wasn't as effective.

You could use the pGH before bed w/ CJC. I wouldn't drop the GHRP-6 but just use a little dose. One study found that using just 30mcg of GHRP-2 w/ GHRH greatly amplified the pulse. So you could use CJC + a litle bit of GHRP-6 + pGH.

The unreconstituted vials of pGH should have a decent shelf-life. Probably the same life as sealed gaba.

But I used a reconstituted half-vial of pGH once that had been on the shelf in reconstituted form for three months and I could tell it had degraded somewhat.

The following paragraphs covering pGH & Slow Wave Sleep were originally written & posted by me as part of my original now defunct thread concerning Growth Hormone Secretagogues.

Originally Posted on 05-28-2008

DatBtrue said:

Night-time GH release and "Slow Wave Sleep" seem to be two sides of the same coin. Increase/decrease one and the other increases/decreases as well.

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I had to go back to your actual research papers, to understand that GHRP and GHRH work through the hypothalamus and the pituitary gland, while GABA/GABOB's effect seems to be directly on the brain, causing prolonged SWS.
The way I understand it, this means the effect of pGH will not interfere with or be neutralized by the effects of GHRP and GHRH. However I am left to wonder whether it's just a compound effect, or a synergistic effect.

I guess I'd have to try the peptides out first, and then add pGH to find out if and what kind of an change in effect will be observed.

On to other possible ways of enhancing the effects of the peptides.

According to the studies, a GH pulse occurs very fast after the beginning of a physical exercise. What happens when a subject is injected with GHRP+/CJC-1295, and engages in physical exercise up to 60 minutes of the injection (while the peptide-induced GH peak is still present)? Will the body produce another pulse, which would result in an increase in the height of the peptide-induced peak, or will it detect the high levels of GH and not produce a pulse? I know you said that GHRP-6 will induce a peak or amplify an existing one, but this situation seems like the other way around.

In the "Adaptation of the 24-h growth hormone profile to a state of sleep debt " by Spiegel K, Leproult R, Colecchia EF, L'Hermite-Balériaux M, Nie Z, Copinschi G, Van Cauter E. from 2000, the researchers found out that:

"In the sleep-debt condition, significant GH secretory pulses were detected at 4 h 14 min ± 18 min after breakfast presentation, at 4 h 22 min ± 20 min after lunch presentation, and at 4 h 1 min ± 19 min after dinner presentation. In the sleep extension condition, significant GH secretory pulses were detected at 4 h 26 min ± 18 min after breakfast presentation and at 4 h 12 min ± 24 min after lunch presentation. Postbreakfast and -lunch GH secretions were similar in both study conditions. Sleep onset occurred on average 3 h 37 min ± 13 min after the evening meal in the sleep-extension condition, i.e., before a postdinner GH pulse could be observed while the subjects were still awake."

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The pattern of a "significant secretory pulse" 4 hours after a meal seems pretty consistent. Here is where I'd ask the same questions as for the previous paragraph - should one inject at the times these postmeal pulses occur, to get 3 augmented peaks, or should one avoid injecting at those times, and hope to get those three postmeal pulses + however many pulses from injections of GHRP-6.

If these questions can be answered, I think I can make an Excel sheet, or a simple computer program, which will give you the optimal times of the day to inject the subject, depending on times the subject can eat and exercise during that day, as input.

likkayouth said:

...According to the studies, a GH pulse occurs very fast after the beginning of a physical exercise. What happens when a subject is injected with GHRP+/CJC-1295, and engages in physical exercise up to 60 minutes of the injection (while the peptide-induced GH peak is still present)? Will the body produce another pulse, which would result in an increase in the height of the peptide-induced peak, or will it detect the high levels of GH and not produce a pulse? I know you said that GHRP-6 will induce a peak or amplify an existing one, but this situation seems like the other way around.

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Here is GH release due to exercise:


Here is a GH pulse with GHRH, a GHRP and GHRH+GHRP in older and younger people:


That natural pulse is 5 ng/ml (or 5 ug/L) vs. the peptide pulse which is as high as 90 ug/L (or 90 ng/ml)

My point is it doesn't matter. It is of almost no significant consequence.

likkayouth said:

In the "Adaptation of the 24-h growth hormone profile to a state of sleep debt " by Spiegel K, Leproult R, Colecchia EF, L'Hermite-Balériaux M, Nie Z, Copinschi G, Van Cauter E. from 2000, the researchers found out that:



The pattern of a "significant secretory pulse" 4 hours after a meal seems pretty consistent. Here is where I'd ask the same questions as for the previous paragraph - should one inject at the times these postmeal pulses occur, to get 3 augmented peaks, or should one avoid injecting at those times, and hope to get those three postmeal pulses + however many pulses from injections of GHRP-6.

If these questions can be answered, I think I can make an Excel sheet, or a simple computer program, which will give you the optimal times of the day to inject the subject, depending on times the subject can eat and exercise during that day, as input.

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In males as much as 80% of 24 hour GH output occurs during that night-time pulse. Other pulses are small.

Here is just a loose graph meant to illustrate the pattern:


There is more to GH and growth then absolute levels.

You are at your most catabolic and really have no GH pulse in the morning so that is a good time to generate one. PWO you are concerned with enhancing nutrient partitioning and opening up more of an anabolic window in the presence of elevated insulin levels and PWO nutrition.

Recovery & growth occurs as we sleep. It is important to maximize GH release at night as our body will benefit from it perhaps more than any other time.

DatBtrue said:

......

My point is it doesn't matter. It is of almost no significant consequence.

In males as much as 80% of 24 hour GH output occurs during that night-time pulse. Other pulses are small.
......

Recovery & growth occurs as we sleep. It is important to maximize GH release at night as our body will benefit from it perhaps more than any other time.

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I see your point.

I was wondering what other GH secretagogues were out there, and came to this article

**broken link removed**

Here's an excerpt from it, a sample list of what the author know about:

GH-Secretagogue: a growth hormone secretagogue, i.e. a substance stimulating growth hormone release, such as ghrelin or a ghrelin-like compound. A GH secretagogue according to the invention may for example be selected from the group of:

L-692-429, L-692-585 (Benzoelactam compounds)

MK677 (Spiroindaner)

G-7203, G-7039, G-7502 (Isonipecotic acid peptidomimetic)

NN703, ipamorelin.

Ardana secretagogue analogue, EP01572

GHRP-1 (Bower)

GHRP-2 (Bower)

GHRP-6 (Bower)

Hexarelin (Europeptide)

Ipamorelin (Novo Nordisk)

NNC 26-0235 (Novo Nordisk)

G-7039 (Genentech)

G-7502 (Genentech)

NNC26-0323 (Genentech)

NN703 (Novo Nordisk)

NNC26-0722(NN) (Novo Nordisk)

L-692,429 (Merck)

L-692,585 (Merck)

NNC26-0610(NN) (Novo Nordisk)

MK-677 (Merck)

L-163,540 (Merck)

CP-424,391 (Pfizer)

EP51319 (Theratechnology)

RC-1291 (Rejuvenon)

BIM28125 (IPSEN)

BIM28131 (IPSEN)

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If one was to acquire any of these, would the protocol of testing them be the same as for GHRP-6?,

xxxxx said:

I had one other question I wanted to ask, even though it is a bit off topic.

What are your thoughts on Hexarelin?

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Hexarelin is very much on topic in the sense that it is one of the growth hormone releasing peptides (GHRPs).

By GHRP I mean a synthetic form of Ghrelin (w/o the negative aspects) capable of binding to the GH-receptor and stimulating GHRH release in the hypothalamus, inhibiting Somatostatin (at both the hypo & pit) & having some direct effects of GH release directly in the pituitary.

All the GHRPs act the same way and create a GH pulse, synergistically so w/ GHRH (CJC-1295).

The literature pretty much treats them all the same.

The differences are:

POTENCY:

• Ipamorelin is potent but the weakest GH releaser.
• GHRP-6 is very potent in effecting GH release.
• GHRP-2 is a little bit more potent then GHRP-6
• Hexarelin, the strongest is a little more potent then GHRP-2.

CORTISOL & PROLACTIN:

• Ipamorelin does not increase cortisol or prolactin at any dose.
• GHRP-6 dose not effect these hormones up to 100mcg but does so minimally above 100mcg.
• GHRP-2 has a stronger effect on these hormones at all dosing levels rising to the high normal range for cortisol & prolactin.
• Hexarelin at all dosing levels has the strongest impact on cortisol & prolactin with levels in the upper bounds of normalcy.

DESENSITIZATION:

• Ipamorelin & GHRP-6 do not desensitize as long as there are short breaks between doses (i.e. 2 hours or so).
• GHRP-2 does not desensitize in the lower dose ranges w/ short breaks. At high dose it is unclear, but some desensitization may occur.
• Hexarelin has been shown to desensitize w/o regard to dose and even with short breaks between doses. This effect shows up after 14 days of continuous use and may be avoided by either keeping doses low or taking a full day or two off every two weeks.

DOSES:

• Saturation dose for all GHRPs is 100mcg or (1mg/kg).
• Effective doses have been demonstrated that are lower (particularly if used w/ GHRH).
• Higher than 100mcg may have an effect but only a fraction of the above 100mcg will be taken up by an available receptor.
• The highest dose in the literature beyond which there was zero benefit is 400mcg.

* Effective of dose is measure by the amount of GH released in plasma as a result. It is not a measure of side-effects or intensity of hunger.

likkayouth said:

If one was to acquire any of these, would the protocol of testing them be the same as for GHRP-6?,

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First of all please don't datadump. A link to the patent article would have been sufficient.

Second I could probably list several hundreds of "growth hormone secreatagogues". Sophisticated computer modeling based on huge chemical & compound libraries can come up w/ all sorts of molecular structures. The majority of those you list are molecular structures that are never intended to ever be any type of end product.

For the most part there is no search for more effective peptides. GHRP-6, GHRP-1 (intermediate peptide not used much, GHRP-2 & Hexarelin followed more recently with Ipamorelin is all that is needed.

These peptidyl structures have benefits beyond mere GH release. They bind to receptors in the thymus & heart, helping to restore some size to the former which is important for immune function and in some instances are cardioprotective in the latter.

They also reduce muscle atrophy by reducing the expression of muscle-specific ubiquitin ligases.

Peptides which are a string of amino acids are too big to be used transdermally and have low oral bioavailability.

Some were also created before the natural ligand Ghrelin was discovered (but it was predicted) and before the growth hormone secreatagogue receptor was modeled (it was known but never seen).

So GHRP-6 was used to begin to do research that would lead to small molecular structures that would both effect GH release and tell the scientists at Merck something about the molecular mechanisms involved. They started with benzoelactam compounds and created many "effective for their purposes" compounds before eventually moving into spiroindaner compounds. MK-677 was an end product "pure" molecular compound from which the structure of GHS-receptor was eventually modeled & discovered.

MK-677 also had high bioavailability (doses I believe were around 25 grams) and it was tested in clinical trials as well. The hope was to create an orally active GHS.

The problem though as I mentioned in my article was that people quickly desensitize to this route of delivery w/ this and most molecular compounds.

In addition it eventually became known that GHS (no matter what their shape or form) were not capable by themselves of elevating IGF-1 high/long enough to effect much growth in GH-deficient children.

Research has continued with other molecular compounds (known as peptidyl-mimetics) that are derived from the peptide Ipamorelin. Many of these compound have demonstrated good oral bioavailability. One or two of these compounds may even be in various phases of clinical trials under various names (for example Pralmorelin, Capromorelin (one of those is a GHRP-2 derivative)) but none will be an FDA approved drug anytime soon.

To directly answer your question though you don't EVER want to inject anything into your body that hasn't been previously tested for toxicity & antibody generation. It is BEST to also not be the first human to introduce a newly created compound to your body.

Just look at what happened to all the U.S. soldiers who were given a certain form of the Anthrax vaccine which used the adjuvant squalene as an immune booster. Many of them developed anti-bodies to squalene which wouldn't be so bad except squalene is present in much of our tissue. So the body begins attacking squalene in its own tissue. The degree to which this happens varies. For some it meant a quick demise for others they will fight various forms of degenerative disease for the rest of their lives and for still others there will be no ill effect.

DatBTrue is the man. Great info brother.

Dat, wow bro, you are one helluva source for information, hats off to you!

I am definitely planning on dosing the GHRP6 @ 200 mcg 3/ day 10-30 minutes before meals (once upon waking, once pre or post workout, and once before bed). I also plan on leaving a shake with protein and natty pbutter in the fridge for night feedings just in case....

Now, as far as the CJC 1295 goes, I think I fall in the same boat as others in terms of economic efficiency. Do you think the optimal dose would be 100 mcgs with my last dose of GHRP6, and if so, how to administer food after to ensure greatest benefit, or the 50 mcg along with every 200 mcg GHRP dose? Thank you for your time and information again....

Grunt76 said:

DatBTrue is the man. Great info brother.

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Thanks bro I appreciate you as well.

Dat, if your last meal before bed contains carbs and fat, is it better to take the ghrp6 10-20min before that meal, or 30min after that meal? Thank you

Max32 said:

...
Now, as far as the CJC 1295 goes, I think I fall in the same boat as others in terms of economic efficiency. Do you think the optimal dose would be 100 mcgs with my last dose of GHRP6, and if so, how to administer food after to ensure greatest benefit, or the 50 mcg along with every 200 mcg GHRP dose? Thank you for your time and information again....

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First off I used 2.1mgs/week of CJC-1295 for the first 6 weeks of my anabolic cycle, then cut it down to about 700mcgs/week for 4 weeks and now I have ramped back up to 2.1mgs/week.

For me it turned out that there was a big difference between the two dosing schemes. 700mcgs/week contributes for sure but my rate of growth slowed down very much & the slin put a little more fat on. I now perceive my growth rate picking back up at the 2.1mcg dose level.

In specific regard to your question, the nighttime dose is the most important because we grow at night, GH increases sleep, and CJC-1295/GHRP-6 amplifies that big nighttime pulse. If I could only dose once it would be pre-bed.

If I could only dose twice it would be post workout & bed.

If I can dose three times it is morning PWO & pre-bed.

During my low dose 4 week period I dosed only 50mcg with GHRP-6 three times a day.

However those times when I skipped a dose and instead used 100mcg pre-bed gave me deeper sleep (and thus a higher GH pulse than did the 50mcgs).

As far as food intake, dose the CJC-1295/GHRP-6 and wait at least 5 minutes up to 30 minutes to give the body a chance to produce GH before eating (which may blunt GH release). I usually wait 30 minutes.

Question for all those who are using cjc. I've only injected twice so far, only cjc, and was wondering if this was normal. About 60 seconds after I inject in the morning, I get pretty hot, and my pulse gets going pretty fast, and pretty hard. I can feel it pulsating in my head. Kind of get a headache as well. Is this normal? Kinda worries me. Let me know, thanks!