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Good writeup. Is my understanding correct that the release of somatostatin is primarily triggered by carb and fat consumption? Gh is released when fasting to mobilize fat cells into the bloodstream to be used as energy for the body when blood glucose is low. Once the body has an alternative fuel source in blood glucose, somatostatin is released to stop GH from releasing fats into the bloodstream. Which is why exogenous GH administration results in high BG as lipolysis continues even when blood glucose is available as energy. Interesting how somatotropin and somatostatin are primarily blood glucose regulators yet it is only known for it's effects on growth.

Also do you believe that GH has any direct effects apart from lipolysis or are all the growth-related effects of GH mediated through it's stimulation of IGF-1?

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Good post, only thing I would change is that CJC-1295 NO DAC is the same as Mod 1-29 so where it says 'No CJC, CJC-1295 (NO DAC) is ok.

 

Kinda off topic but what are your thoughts on PEG-MGF vs MGF? 

 

 

The science of MGF may not apply to exogenous MGF. The reason... there may not be an MGF receptor and there may be not way that the cell can internalize exogenous MGF. Scientists disagree, because there was no proven way for exogenous MGF to act within the cell. .. it's just that some of the science started indicating that some intracellular signaling was occurring that was proliferative. One camp is adamant that this is not the case. I can't say that exogenous acts as native MGF.? 

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Good post, only thing I would change is that CJC-1295 NO DAC is the same as Mod 1-29 so where it says 'No CJC, CJC-1295 (NO DAC) is ok.

 

 

Here's something I've pulled out:

GHRH is a 44 amino acid peptide. It binds to its native receptor on the membrane of somatrophs and brings about GH release. [To be very, very complete sometimes GHRH shows up as a 40 amino acid peptide]

Now the final 15 amino acids of GHRH are unnecessary to bind and activate the GHRH receptor, so in the lab they have been left off and only the first 29 are kept. This was named GRF(1-29). This stands for Growth Hormone Releasing Factor and the 1-29 means amino acids from position 1 to 29 of GHRH were retained.

GRF(1-29) was named Sermorelin by a pharmaceutical company. GRF(1-29) binds to the GHRH receptor as well as GHRH does.

Now if you inject GRF(1-29) into the blood streams enzymes will quickly cleave the peptide at the 2nd position. So GRF(1-29) was altered at the 2nd position to prevent this. That alteration was replacing alanine with its isomer D-alanine. D-Ala2 GRF(1-29) binds to the GHRH receptor as well as GHRH does.

Now to make GRF(1-29) even more resilient 3 more amino acids were changed, brining the total changes to four (tetra - the Greek cardinal number 4). So a tetra subbed GRF(1-29) is GRF(1-29) with replacements at the 2nd, 8th, 15th & 27th amino acids positions. This also has come to be known as "Modified GRF(1-29)". Modified GRF(1-29) binds to the GHRH receptor as well as GHRH does.

Now a company called ConjuChem Biotechnologies Inc. came up with a drug. A drug called a "drug affinity complex" (DAC). This complex attaches to albumin in plasma. So they experimented with it by attaching it to insulin and glucagon-like peptide-1. Those were there two primary products. Along the way they also experimented with attaching it to various forms of GRF(1-29). They attached it to an added lysine (called a linker) which was attached to GRF(1-29) and called this CJC (after ConjuChem) plus the number 1288 (CJC-1288) to compare with attaching it to an added lysine (called a linker) which was attached to D-Ala2 GRF(1-29) which was called CJC-1293 to compare with attaching it to an added lysine (called a linker) which was attached to Modified GRF(1-29) which was called CJC-1295.

All of these Drugs (CJC-1288, CJC-1293, CJC-1295) binds to the GHRH receptor as well as GHRH does. ConjuChem Biotechnologies Inc. stopped experimenting clinically after a member of the study group died. ConjuChem Biotechnologies Inc. also saw the worthlessness of this product and focused on the insulin and GLP-1 product (called Exendin-4).

Unfortunately ConjuChem Biotechnologies Inc's product (drug affinity complex) had no commercial value. They filed for bankruptcy on 7/21/2010 in Canada under the Bankruptcy and Insolvency Act.

Now the banner ad retailers somehow all where lied to by the Chinese and years ago were selling CJC-1295 however it was not CJC-1295. It usually was plain old GRF(1-29). When they were called on it they created phony COAs for customers. However years ago we came to understand that CJC-1295 results in growth hormone bleed. You don't actually bleed.. What happens is you elevate troughs and the trough to peak pulsation is of reduced amplitude... and you end up with GH oozing out in more "urinating in the pool" fashion as opposed to the "squid ink" more desirable pattern.

So years ago we determined that CJC-1295 was not desirable but modified GRF(1-29) was desirable. The banner ad retailers after the early rounds of lying eventually made demands of their Chinese suppliers and they eventually produced some CJC-1295. So that is what they sold. The CJC to them was a premium label so when people demanded that they sell them something useful they just attached the CJC moniker to everything. They then threw in the "w/o DAC". Then they got really confused and started with CJC-1293 w/o DAC. They never realize that CJC-1293 would indicate that they have only that one modification at the 2nd position D-Ala2 GRF(1-29) + lysine + DAC.

When they throw in the term "w/o DAC" they are indicating that they are selling D-Ala2 GRF(1-29) + an unstable lysine.

Confused? You should be..lol

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Good post, only thing I would change is that CJC-1295 NO DAC is the same as Mod 1-29 so where it says 'No CJC, CJC-1295 (NO DAC) is ok.

 

Kinda off topic but what are your thoughts on PEG-MGF vs MGF? 

 

 

The science of MGF may not apply to exogenous MGF. The reason... there may not be an MGF receptor and there may be not way that the cell can internalize exogenous MGF. Scientists disagree, because there was no proven way for exogenous MGF to act within the cell. .. it's just that some of the science started indicating that some intracellular signaling was occurring that was proliferative. One camp is adamant that this is not the case. I can't say that exogenous acts as native MGF.? 

There are heappps of pubmed studies that use exogenous MGF with a positive result over control

 

regarding CJC1295 NO DAC, getting into semantics here. I think the conclusion is it works just as well as mod 1-29 and is usually labelled as the same product.

 

 

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Hey TKav (and welcome).

That's actually a good point. HGH is prescription, isn't it? But these are peptide fragments, and classed as "research chemicals", right?

Although I beleive MedSafe is still able to class research chemicals as a medicine, if they think it's going to be used in the manner of a medicine.

And yeah, we had a good discussion on that NZ Herald article when it first came out. Looking at it again now, I'm remembering all over again how much it annoyed me the first time!

 

Confused? You should be..lol

Very!

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Thanks sorry I should have introduced myself, new member here.
Im 99.9% sure they arent legal, unless you get some letter from medsafe stating they are for research use. I may be wrong...after reading that article I got quite interested in them (research geek) and discovered they are quite readily available in NZ, and for a while seemed to be a new craze. This is coming from someone with ZERO experience in this area, but they kept popping up more and more in differing conversations among differing groups of people.

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