Whats the latest dosing protocol with GHRP-2+MOD GRF 1-29?

[Knight9]

It used to be 100/100 but it seems that the tune for the saturation dose has changed? I am going to run 3x per day..upon waking, post workout, and before bed...10 min before Rips GH. Input appreciated!

 

[bencozzy]

The ghrp-6 and 2 are still 100 but mod grf can go up to 200.

 

[Knight9]

Without desensitization? Is 200 twice as good or is it non linear?

 

[sammy555]

100 is still situation dose for both, but that doesn't mean you can't go higher, its just diminishing returns. Even the boom dosers that do 1mg of ipam or ghrp2 still use only 100 mod grf. Increase your ghrp not your ghrh

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[Knight9]

2 posts and they are contradicting...shit

 

[sammy555]

2 posts and they are contradicting...shit

Mabey so but mine is correct, do some research and you will see. I suggest you sign up at datbtrue and have a good read.

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[ldog40]

2 posts and they are contradicting...shit

I'd take Sammy's word, any day over bencozzy. Being a newbie doesn't necessarily mean he is wrong, but in this case he definitely is.

A simple reading of various posts and threads and DatBTrue's board (as Sammy said) proves it.

 

[bmit]

Running 300 mcg GHRP-2 and 125 mcg CJC-1295. Both 3-4 x day. Cheap too to do. Also taking 150 mcg T4 on M-F

 

[sammy555]

Running 300 mcg GHRP-2 and 125 mcg CJC-1295. Both 3-4 x day. Cheap too to do. Also taking 150 mcg T4 on M-F

Sounds good, care to share results. GHRP2 screws with my sleep and do does 6 to a degree

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[wardog50]

My subject uses 400 mics of ghrp and 100 of ghrh.
I think the ghrh could go substantialy higher in testing.

 

[THE-DET-OAK]

100 is still situation dose for both, but that doesn't mean you can't go higher, its just diminishing returns. Even the boom dosers that do 1mg of ipam or ghrp2 still use only 100 mod grf. Increase your ghrp not your ghrh

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^^^ yup

 

[johnjuanb1]

It used to be 100/100 but it seems that the tune for the saturation dose has changed? I am going to run 3x per day..upon waking, post workout, and before bed...10 min before Rips GH. Input appreciated!

GHRP-2 doesn't have a typical saturation dose like other GHRP's. I have been giving my research rat a BOOM dose of 1,000mcg 2-3x/day for weeks with no desensitization of the pituitary. It still hits him like a ton of bricks. Here is an abstract demonstrating the potency of GHRP-2.

The Effect of GH-Releasing Peptide-2 (GHRP-2 or KP 102) on GH Secretion from Primary Cultured Ovine Pituitary Cells Can be Abolished by a Specific GH-Releasing Factor (GRF) Receptor Antagonist

1. Danxing Wu,
2. Chen Chen,
3. Kazuo Katoh,
4. Jin Zhang and
5. Iain J. Clarke

Abstract

A newly synthesised GH-releasing peptide, KP 102 (also named GHRP-2), was studied in an in vitro perifusion system of primary cultured ovine anterior pituitary cells. Application of KP 102 to the perifusion medium caused a dose-dependent increase in GH secretion. Dose-response relationships indicated that KP 102 had similar potency to GRF and was 10-fold more potent than earlier generations of GH-releasing peptide (GHRP-6 and GHRP-1) tested in same system. The response to a second application of KP 102 given within 1 h of initial application was significantly lower than the response to the first application. When KP 102 (or GRF) was applied first and then GRF (or KP 102) given 1 h later, the second response was not attenuated. When GRF and KP 102 were coadministered, an additive effect on release of GH was obtained. The effect of maximal dose of KP 102 (100nM) on GH release was totally abolished by [Ac-Tyr1, d-Arg2] GRF 1-29 (1μM) which is believed to be a specific antagonist for the GRF receptor. Blockade of Ca2+ channels by Cd2+ (2mM) diminished the basal GH secretion and abolished the increase in GH release in response to KP 102 (100nM). These data suggest that the action of KP 102 is blocked by a GRF receptor antagonist and therefore acts through a different receptor to that employed by earlier generations of GH-releasing peptides. GH release in response to KP 102 involves an increase in Ca2+ influx and there is no cross-desensitization between KP 102 and GRF responses.

 

[rock75]

GHRP-2 doesn't have a typical saturation dose like other GHRP's. I have been giving my research rat a BOOM dose of 1,000mcg 2-3x/day for weeks with no desensitization of the pituitary. It still hits him like a ton of bricks. Here is an abstract demonstrating the potency of GHRP-2.

The Effect of GH-Releasing Peptide-2 (GHRP-2 or KP 102) on GH Secretion from Primary Cultured Ovine Pituitary Cells Can be Abolished by a Specific GH-Releasing Factor (GRF) Receptor Antagonist

1. Danxing Wu,
2. Chen Chen,
3. Kazuo Katoh,
4. Jin Zhang and
5. Iain J. Clarke

Abstract

A newly synthesised GH-releasing peptide, KP 102 (also named GHRP-2), was studied in an in vitro perifusion system of primary cultured ovine anterior pituitary cells. Application of KP 102 to the perifusion medium caused a dose-dependent increase in GH secretion. Dose-response relationships indicated that KP 102 had similar potency to GRF and was 10-fold more potent than earlier generations of GH-releasing peptide (GHRP-6 and GHRP-1) tested in same system. The response to a second application of KP 102 given within 1 h of initial application was significantly lower than the response to the first application. When KP 102 (or GRF) was applied first and then GRF (or KP 102) given 1 h later, the second response was not attenuated. When GRF and KP 102 were coadministered, an additive effect on release of GH was obtained. The effect of maximal dose of KP 102 (100nM) on GH release was totally abolished by [Ac-Tyr1, d-Arg2] GRF 1-29 (1μM) which is believed to be a specific antagonist for the GRF receptor. Blockade of Ca2+ channels by Cd2+ (2mM) diminished the basal GH secretion and abolished the increase in GH release in response to KP 102 (100nM). These data suggest that the action of KP 102 is blocked by a GRF receptor antagonist and therefore acts through a different receptor to that employed by earlier generations of GH-releasing peptides. GH release in response to KP 102 involves an increase in Ca2+ influx and there is no cross-desensitization between KP 102 and GRF responses.

???? what's that mean exactly...first is says it had an additive effect on release of GH, but then says it was totally abolished -

 

[sammy555]

???? what's that mean exactly...first is says it had an additive effect on release of GH, but then says it was totally abolished -

These fucking studies never end like they should. They should always end with - so in layman terms...............................

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[johnjuanb1]

???? what's that mean exactly...first is says it had an additive effect on release of GH, but then says it was totally abolished -

I see your point. HAHAHA...not sure what that means. DAMN!!!

 

[Medic08]

JJ1, when you say, "it's hits me like a ton of bricks," what are you referring to??? Heat flash, hypo, hunger??? Just curious.

 

[rock75]

I see your point. HAHAHA...not sure what that means. DAMN!!!

LOL, just had me scratching my head that's all.

When GRF and KP 102 were coadministered, an additive effect on release of GH was obtained. The effect of maximal dose of KP 102 (100nM) on GH release was totally abolished by [Ac-Tyr1, d-Arg2] GRF 1-29 (1μM) which is believed to be a specific antagonist for the GRF receptor.

I think it is saying that GRF 1-29 (which is what we are researching) abolished (diminished) GH release....which contradicts what we've all thought...:banghead:

so if that is in fact the case what other GRF antagonist(s) are better for Increasing GH release?? or am i over analyzing this and making shit more complicated (LOL, now i feel like ronnie)

 

[johnjuanb1]

JJ1, when you say, "it's hits me like a ton of bricks," what are you referring to??? Heat flash, hypo, hunger??? Just curious.

I get a head rush. Sometimes I have to lie down. I often want to take a nap.

 

[wardog50]

LOL, just had me scratching my head that's all.

When GRF and KP 102 were coadministered, an additive effect on release of GH was obtained. The effect of maximal dose of KP 102 (100nM) on GH release was totally abolished by [Ac-Tyr1, d-Arg2] GRF 1-29 (1μM) which is believed to be a specific antagonist for the GRF receptor.

I think it is saying that GRF 1-29 (which is what we are researching) abolished (diminished) GH release....which contradicts what we've all thought...:banghead:

so if that is in fact the case what other GRF antagonist(s) are better for Increasing GH release?? or am i over analyzing this and making shit more complicated (LOL, now i feel like ronnie)

I'm reading that different or something.
To me it says that when administered together the growth hormone released increased.
The part that seems to be confusing is where it says the abolished thing. I think there they are saying it abolished the maximal dose. In other words now when administered together dosing could go higher because the wall that didn't allow more release at higher dosing was now broken down by using both together.
So the max dose rule is what is abolished actually allowing for higher doses and higher hgh output.

Thats what I'm getting from it anyway.

 

[THE-DET-OAK]

I'm reading that different or something.
To me it says that when administered together the growth hormone released increased.
The part that seems to be confusing is where it says the abolished thing. I think there they are saying it abolished the maximal dose. In other words now when administered together dosing could go higher because the wall that didn't allow more release at higher dosing was now broken down by using both together.
So the max dose rule is what is abolished actually allowing for higher doses and higher hgh output.

Thats what I'm getting from it anyway.

I agree.

I think it abolished the saturation dose.

If you look at script grade the combo is dosed at 200 (GHRH) 200 (GHRP - 6) 500 (GHRP-2) because GHRP-2 does have a higher saturation dose.

L-Arginine has also been proven to improve the pulse when used in conjunction with GHRP-2