IGF-1 LR3 effects on serum IGF-1 levels?

James Bond12

New Member
To what extent does IGF-1 LR3 increase serum IGF-1 levels? If anyone has ever gotten their IGF-1 levels tested while taking IGF-1 LR3, I'd love to hear about your experiences.
 
If anything, it decreases serum IGF-I.
Explain in depth if you can. I am coming from a forum who's cannot decide/figure out whether IGF-1 LR3 would be effective in pushing your IGF-1 levels further after they have stagnated after a specific threshold of HGH use.

And if IGF-1 LR3 is ineffective at increasing serum IGF-1 levels, is there any variant of IGF-1 (non-recombinant or DES) that actually helps raise IGF-1 levels?
 
Explain in depth if you can. I am coming from a forum who's cannot decide/figure out whether IGF-1 LR3 would be effective in pushing your IGF-1 levels further after they have stagnated after a specific threshold of HGH use.

And if IGF-1 LR3 is ineffective at increasing serum IGF-1 levels, is there any variant of IGF-1 (non-recombinant or DES) that actually helps raise IGF-1 levels?
These are really good questions. I would love to know those answers as well. All I can say is that even though I’m on GH peptides that have raised my igf1 levels…I was on a plateau that igf1 des certainly helped overcome…but I also used peg MGF at the same time. I have been using Lr3 the last 6 weeks…2-3 days a week and then Peg about 2 days a week (30 hours after lr3 pins). I hit a PR yesterday which added 20 pounds to my bench. I’m going to state from my own testing that although I was on lr3 yesterday….which may have been my best chest workout ever….however I think it was because the two previous off days one of which Peg MGF that permitted me to heal. Not sure if this helps your good questions….but lr3 is certainly giving me a nice boost but I’m trying to learn more like you.
 
Explain in depth if you can. I am coming from a forum who's cannot decide/figure out whether IGF-1 LR3 would be effective in pushing your IGF-1 levels further after they have stagnated after a specific threshold of HGH use.

And if IGF-1 LR3 is ineffective at increasing serum IGF-1 levels, is there any variant of IGF-1 (non-recombinant or DES) that actually helps raise IGF-1 levels?
RhIGF-I (mecasermin; e.g., Increlex) is the only IGF that will increase serum IGF-I.

LR3 IGF-I is a different peptide. It is an analogue of IGF-I that contains a 13-amino acid extension at the NH₃-terminal end consisting of Met-Phe-Pro-Ala-Met-Pro-Leu-Ser-Ser-Leu-Phe-Val-Asn and has an arginine substitution for a glutamic acid at residue 3. As a result, it is resistant to IGFBP binding, dramatically reducing its biological half-life, and necessitating frequent multiple daily injections to achieve any biological effect (marked by hypoglycemia on par with rhIGF-I).

The reason that you should expect, if anything, reduced serum IGF-I concentrations on bloodwork is because LR3 in most assays is not crossreactive with IGF-I, & because it rapidly clears circulation due to lack of IGFBP binding.

Here is evidence of it lowering serum IGF-I: Gehrig SM, Ryall JG, Schertzer JD,Lynch GS. Insulin-like growth factor-I analogue protects muscles of dystrophic mdx mice from contraction-mediated damage. Exp Physiol. 2008 Nov;93(11):1190-8. doi: 10.1113/expphysiol.2008.042838. Epub 2008 Jun 20. PMID: 18567600.

Other notable effects were that, given continuous 24-h infusion in rats, it had no significant effect on muscle contractile properties, mass, force capacity,
nor specific force, it decreased median myofiber cross-sectional area, indicating that IGFBP interaction is needed to maintain or augment muscle myofiber size.
 
Zero effects on serum igf1. I have tried both: human igf1 and igf1lr3

Igf1lr3 may bind to igf1 receptors on muscle and intestine, but zero effects on serum igfbp3 or igf1

And I would test igfdes because its closer to igf1 not lr3
 
The reason that you should expect, if anything, reduced serum IGF-I concentrations on bloodwork is because LR3 in most assays is not crossreactive with IGF-I, & because it rapidly clears circulation due to lack of IGFBP binding.

Here is evidence of it lowering serum IGF-I:

Do you suspect this is due to negative feedback inhibition from LR3? Since increlex is IGF-1, it replaces any theoretical endogenous IGF-1 inhibition. LR3 does the inhibition but doesn't cross react so IGF-1 replacement is not detected?
 
Its a disappointing peptide for sure. If it did what it was hyped up to do, it would be solid. But i havent seen any Solid evidence, even solid anecdotal evidence (at best) besides solid pumps in the gym.

That counts for something ! But not much overall.
 
Its a disappointing peptide for sure. If it did what it was hyped up to do, it would be solid. But i havent seen any Solid evidence, even solid anecdotal evidence (at best) besides solid pumps in the gym.

That counts for something ! But not much overall.

Its a good GDA, but I would stick on Lantus due to safety
 
Do you suspect this is due to negative feedback inhibition from LR3? Since increlex is IGF-1, it replaces any theoretical endogenous IGF-1 inhibition. LR3 does the inhibition but doesn't cross react so IGF-1 replacement is not detected?
If it's lowered in man, it must be due to negative feedback inhibition. Not surprising, every hormone does this at least acutely.
 
RhIGF-I (mecasermin; e.g., Increlex) is the only IGF that will increase serum IGF-I.

LR3 IGF-I is a different peptide. It is an analogue of IGF-I that contains a 13-amino acid extension at the NH₃-terminal end consisting of Met-Phe-Pro-Ala-Met-Pro-Leu-Ser-Ser-Leu-Phe-Val-Asn and has an arginine substitution for a glutamic acid at residue 3. As a result, it is resistant to IGFBP binding, dramatically reducing its biological half-life, and necessitating frequent multiple daily injections to achieve any biological effect (marked by hypoglycemia on par with rhIGF-I).

The reason that you should expect, if anything, reduced serum IGF-I concentrations on bloodwork is because LR3 in most assays is not crossreactive with IGF-I, & because it rapidly clears circulation due to lack of IGFBP binding.

Here is evidence of it lowering serum IGF-I: Gehrig SM, Ryall JG, Schertzer JD,Lynch GS. Insulin-like growth factor-I analogue protects muscles of dystrophic mdx mice from contraction-mediated damage. Exp Physiol. 2008 Nov;93(11):1190-8. doi: 10.1113/expphysiol.2008.042838. Epub 2008 Jun 20. PMID: 18567600.

Other notable effects were that, given continuous 24-h infusion in rats, it had no significant effect on muscle contractile properties, mass, force capacity,
nor specific force, it decreased median myofiber cross-sectional area, indicating that IGFBP interaction is needed to maintain or augment muscle myofiber size.
Why do people bring IGF-1 LR3 even in the same sentence as HGH if this has always been the case?

Do you think exogenous insulin usage could raise serum IGF-1 levels then instead
 
Why do people bring IGF-1 LR3 even in the same sentence as HGH if this has always been the case?
Basic confusion stemming from early excitement (and misunderstand basic research studies) generated by BassKillerOnline.

LR3 IGF-I in in vitro data, which is much of what exists since it's not intended for human use & never has been studied in man, has 4- to 5-fold greater affinity for binding to the IGF-IR than IGF-I.

However, in a human skeletal muscle line, it is merely equipotent in stimulating differentiation to IGF-I.

LR3 IGF-I is also resistant to IGFBP binding, which was optimistically, but mistakenly believed to confer greater potency. IGFBPs were viewed simplistically by laypersons as acting analogously to binding proteins to testosterone like SHBG.

However, the IGFBPs modulate IGF activity by extending the half-life of the IGFs and by either potentiating or inhibiting binding of the IGFs to their receptors.

In the end, there is a narrow use case for LR3 IGF-I. It can be used rationally by those who have maximally hypertrophied their available pool of myofibers to increase that pool.
Do you think exogenous insulin usage could raise serum IGF-1 levels then instead
Of course.

Insulin is also more muscle protein anabolic per-IU/mg than IGF-I.

IGF-I & its analogues (e.g., LR3) acts predominantly to stimulate muscle cell proliferation & differentiation (mitogenic & myogenic effects).
 
Do you suspect this is due to negative feedback inhibition from LR3? Since increlex is IGF-1, it replaces any theoretical endogenous IGF-1 inhibition. LR3 does the inhibition but doesn't cross react so IGF-1 replacement is not detected?
I saw you tried qsc lr3? how does it stack up at high doses?
 
I've tried a few sources. Maybe they're all really from the same source (?), but I like LR3 and haven't noticed any big differences between vendors.
I found a source that is 200usd for 20mg I am asking them for a coa I hope what you are saying is true, of I could get 90% dosed, 100% purity lr3 I would be very happy
 
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