Peptigrade

Growth & Metabolic

IGF-1

Insulin-like Growth Factor 1 — 70-amino-acid single-chain polypeptide (recombinant human mecasermin is the FDA-approved form; IGF-1 LR3 is a synthetic long-R3 analog with Arg3→Glu and a 13-residue N-terminal extension)·Also known as: Mecasermin, Increlex, rhIGF-1, Somatomedin C, IGF-I, IGF-1 LR3, Long R3 IGF-1

FDARegulatory status

Recombinant human IGF-1 (mecasermin, brand name Increlex) is FDA-approved since 2005 for long-term treatment of growth failure in children with severe primary IGF-1 deficiency (height SDS ≤ −3 and IGF-1 SDS ≤ −3 with normal/elevated GH) and for patients with GH gene deletion who have developed neutralizing antibodies to GH. All other uses (anti-aging, muscle hypertrophy, body composition, sport performance, neuroprotection) are off-label or unapproved. The IGF-1 LR3 analog circulating in research-chemical channels is not FDA-approved for any indication.

WADARegulatory status

Prohibited at all times (S2 — Peptide Hormones, Growth Factors, Related Substances and Mimetics) on the 2026 WADA Prohibited List (in force January 1, 2026). IGF-1, its analogs (including LR3), and IGF-1 mimetics are explicitly listed.

Regulatory note ·Increlex carries a boxed warning for intracranial hypertension and requires monitoring for hypoglycemia (because IGF-1 binds the insulin receptor with ~0.1× the affinity of insulin but reaches therapeutic concentrations far above physiologic). A separate FDA black-box concern: an observed signal for benign intracranial hypertension and lymphoid tissue hypertrophy in the pediatric trial cohort. IGF-1 LR3 sold as research chemical has no FDA review, no cGMP manufacturing requirement, and no human PK/safety data independent of the mecasermin label. Today is 2026-04-20.

§ The quick take

TL;DR · Editor’s summary

IGF-1 is a tale of two molecules. As mecasermin (Increlex), recombinant human IGF-1 holds an A grade for a single, narrow indication: severe primary IGF-1 deficiency in children with short stature, where FDA-approved 2005 and supported by Chernausek 2007 and Backeljauw 2013 open-label multi-year trials showing first-year height velocity rising from roughly 2.8 to 8.0 cm/year with sustained gains over 8 years of treatment. For that indication, under endocrinologist supervision, it is a legitimate therapy. For everything else, the evidence collapses.

No randomized placebo-controlled trial has demonstrated efficacy of systemic IGF-1 or the IGF-1 LR3 analog for muscle hypertrophy, strength, body composition, or anti-aging in healthy adults. Two adequately-powered ALS trials (Lai 1997; Sorenson 2008, n=330) failed. TBI trials (Hatton 2006) showed metabolic but not functional benefit. The mechanistic case (PI3K–Akt–mTOR activation, satellite-cell recruitment, Rommel 2001; Barton-Davis 1998 viral overexpression) is strong on paper but has never cleared a human efficacy bar outside the rare-disease label.

Worse, the cancer signal is not theoretical: Renehan 2004 meta-analysis across 21 prospective cohorts links high circulating IGF-1 to colorectal, breast, and prostate cancer; IGF-1R drives proliferation and anti-apoptosis in most solid tumors; and Laron-syndrome patients with congenitally low IGF-1 show markedly reduced cancer and diabetes incidence (Guevara-Aguirre 2011). Reduced IGF-1 signaling extends lifespan in nearly every model organism tested. Sold as research chemical, IGF-1 LR3 has no FDA review, no cGMP requirement, no human PK independent of the mecasermin label, and is WADA-prohibited at all times (S2). The A grade attaches to a specific pediatric endocrine diagnosis; the mainstream off-label use cases range from D to F.

§ Grade matrix

The grade
per outcome.

One peptide can earn very different grades for different uses. Here is every outcome we’ve graded for IGF-1, sorted by strength of evidence.

A

Severe primary IGF-1 deficiency (pediatric growth failure)

Strong

FDA-approved indication for mecasermin (Increlex, 2005). Multi-year open-label pediatric trials (Chernausek 2007; Backeljauw 2013) in severe primary IGFD demonstrated mean first-year height velocity increases from ~2.8 cm/yr to ~8.0 cm/yr, with sustained height gain over 8 years. Treatment is endocrinologist-supervised with twice-daily subcutaneous dosing at 0.04–0.12 mg/kg.

12 studiesUpdated 2026-04-20
C

Severe insulin resistance / extreme type A and type B insulin resistance syndromes

Mixed

Multiple small open-label studies (reviewed in Clemmons 2007) in severe syndromic insulin resistance show IGF-1 lowers HbA1c and exogenous insulin requirement. Mecasermin rinfabate (IGF-1 + IGFBP-3) Phase II trials in adult T1D/T2D (1–2 mg/kg/day × 14 days) improved glycemic control. No Phase 3 in common type 2 diabetes; this is a rare-disease signal, not a mainstream metabolic therapy.

9 studiesUpdated 2026-03-28
D

Muscle hypertrophy / body composition in healthy adults

Weak

Mechanistic case is strong (PI3K–Akt–mTOR activation, satellite-cell recruitment, FOXO suppression of E3 ligases — Rommel 2001; Barton-Davis 1998 viral overexpression). No randomized placebo-controlled trial of systemic IGF-1 or IGF-1 LR3 in healthy adults for muscle mass or strength has been published. Off-label bodybuilding use is common but evidence-free.

4 studiesUpdated 2026-03-10
D

Sarcopenia / age-related muscle loss

Weak

Observational cohorts (NHANES III) link low IGF-1 to worse musculoskeletal aging, but a U-shaped relationship exists — high IGF-1 is also associated with risk. No published RCT of exogenous IGF-1 for sarcopenia endpoints in older adults.

3 studiesUpdated 2026-02-22
D

Traumatic brain injury / neuroprotection

Weak

Transgenic mouse overexpression reduced acute hippocampal neurodegeneration post-TBI (Madathil 2013). Phase II human trials of IGF-1 combined with IGFBP-3 in moderate-to-severe TBI (Hatton 2006) showed nitrogen retention but no durable functional benefit. Conflicting long-term data: sustained IGF-1 signaling was pro-epileptic in rodents (Song 2016).

6 studiesUpdated 2026-02-15
F

ALS (amyotrophic lateral sclerosis)

Disproven / Unsafe

Two adequately-powered RCTs of subcutaneous mecasermin in ALS (Lai 1997; Sorenson 2008) produced conflicting then null results. The 2008 Sorenson trial (n=330, 2 years) found no benefit on Appel ALS rating or survival. IGF-1 is not indicated for ALS.

4 studiesUpdated 2026-02-05
F

Anti-aging / longevity

Disproven / Unsafe

Mechanistically contra-indicated. Reduced IGF-1 signaling extends lifespan in nearly every model organism tested (Kenyon 2010). Laron-syndrome humans (IGF-1-deficient) show markedly reduced cancer and diabetes incidence. Exogenous IGF-1 for longevity is directionally wrong by the best available evidence.

5 studiesUpdated 2026-01-30
F

Cancer risk signal (across all off-label uses)

Disproven / Unsafe

High circulating IGF-1 is prospectively associated with increased risk of colorectal, breast, and prostate cancer (Renehan 2004 meta-analysis of 21 studies). IGF-1R activation drives proliferation and anti-apoptosis in most solid tumors. The Increlex label carries warnings; off-label chronic dosing in healthy adults is the highest-concern use pattern.

14 studiesUpdated 2026-01-20

§ Why this grade

Sub-scores for this outcome.

Severe primary IGF-1 deficiency (pediatric growth failure)

Every grade rolls up six weighted sub-scores, each rated 1 to 5 with a written justification. Here is how the top-outcome grade was constructed.

Mechanism understood

5 / 5

IGF-1R → IRS-1 → PI3K/Akt/mTOR and Ras/MAPK/ERK cascades are among the most thoroughly characterized growth-factor pathways in biology (reviewed Hakuno & Takahashi 2018). IGFBP family and ALS ternary-complex regulation are well-documented. Receptor identified, crystal structures available, downstream effectors mapped.

Human studies (count + quality)

4 / 5

FDA approval supported by multi-year open-label pediatric trials (Chernausek 2007, Backeljauw 2013 8-year extension). The limitation that holds this below 5 is the absence of a placebo-controlled Phase 3 — historical controls and within-subject height-velocity comparisons were accepted given the rarity and natural history of severe primary IGFD.

Effect vs placebo

4 / 5

Pre-treatment height velocity ~2.8 cm/yr rising to ~8.0 cm/yr in year 1 is a clinically meaningful effect size against the natural history of the disease. No placebo arm. Effect sustained over 8 years of treatment with height SDS improvement.

Long-term safety data

3 / 5

Increlex post-approval surveillance and the 8-year Backeljauw 2013 cohort provide the longest published exposure. Known adverse events: hypoglycemia, intracranial hypertension, lymphoid tissue hypertrophy, injection-site reactions. Adequate for the approved pediatric indication; not generalizable to adult off-label use.

Side effect profile

3 / 5

Boxed warning for intracranial hypertension. Hypoglycemia is the most common dose-limiting toxicity (insulin-receptor cross-binding at therapeutic concentrations). Tonsillar and adenoidal hypertrophy documented in pediatric cohort. For a drug treating a life-altering deficiency, risk/benefit is acceptable; for off-label use in healthy adults, the same adverse events become unacceptable.

Regulatory status

5 / 5

FDA-approved since 2005 (Increlex, mecasermin) for the graded indication. EMA-approved. This is the only sub-score where IGF-1 earns a full 5 — and only for this specific pediatric endocrine diagnosis. WADA-prohibited at all times (S2); this does not affect the therapeutic-use grade for the approved indication but is disqualifying for sport.

§ What the science says

How IGF-1
works.

Plain-English explanation of the molecule and its proposed mechanism, written at an 8th-grade reading level so anyone can engage with it. Every claim is linked to a primary source below.

What it is

IGF-1 is a 70-amino-acid single-chain polypeptide hormone (MW 7,649 Da, CAS 67763-96-6, UniProt P05019) that mediates most of the growth-promoting effects of pituitary growth hormone. It shares roughly 50% sequence homology with proinsulin — positions 1–29 map to the insulin B chain, 42–62 to the A chain, with a unique C-domain connecting peptide and a D-domain octapeptide extension not present in insulin. Three intramolecular disulfide bridges (6–48, 18–61, 47–52) stabilize the tertiary structure required for IGF-1R binding. The FDA-approved human therapeutic is mecasermin — non-glycosylated recombinant human IGF-1 produced in E. coli, marketed as Increlex (Ipsen). The research-chemical variant most commonly seen in off-label contexts is IGF-1 LR3 (Long R3 IGF-1), a synthetic analog with an Arg3→Glu substitution and a 13-residue N-terminal extension that reduces IGFBP binding and extends plasma half-life; LR3 is not FDA-approved for any indication and has no human PK data in peer-reviewed literature.

How it works

  1. 01

    IGF-1R autophosphorylation and receptor engagement

    IGF-1 binds the type-1 IGF receptor (IGF-1R), a heterotetrameric transmembrane tyrosine kinase with ~50% homology to the insulin receptor. Binding triggers autophosphorylation at Tyr1131/1135/1136 in the kinase domain and Tyr950 in the juxtamembrane region (reviewed in Hakuno & Takahashi 2018). At pharmacologic concentrations, IGF-1 cross-binds the insulin receptor with roughly 0.1× the affinity of insulin — the basis for the hypoglycemia risk in the Increlex label.

  2. 02

    PI3K–Akt–mTOR: the anabolic arm

    Activated IGF-1R phosphorylates IRS-1, which recruits PI3K, generating PIP3, recruiting PDK1, and phosphorylating Akt at Thr308 (full activation requires Ser473 phosphorylation by mTORC2). Akt phosphorylates GSK3β (relieving inhibition of protein synthesis), FOXO1/3/4 (suppressing transcription of the E3 ligases MuRF1 and atrogin-1/MAFbx that mediate ubiquitin-proteasome muscle proteolysis), and TSC2 (activating mTORC1 → p70S6K, 4E-BP1, cap-dependent translation). This is the molecular basis for the anti-atrophy signal documented by Rommel 2001 (Nat Cell Biol) and Sandri 2004 (Cell).

  3. 03

    Ras–MAPK–ERK: the proliferative arm

    In parallel, phosphorylated IGF-1R engages SHC, which recruits Grb2/SOS, activates Ras GTPase, and drives the Raf → MEK → ERK cascade. ERK signaling predominantly governs proliferation and differentiation. The co-activation of PI3K–Akt (survival/growth) and Ras–MAPK (proliferation) is the mechanistic reason IGF-1R is a recognized driver in most solid tumors and the reason anti-IGF-1R monoclonal antibodies have been developed as oncology agents (e.g., figitumumab, ganitumab — both abandoned for efficacy, but the mechanistic concern stands).

  4. 04

    Satellite-cell activation and muscle hypertrophy in animal models

    Barton-Davis 1998 (PNAS) used viral-mediated local IGF-1 gene transfer to mouse hindlimb and showed significant muscle mass and strength gains; gamma-irradiation of satellite cells eliminated ~50% of the effect, implying the remainder came from direct effects on differentiated myofibers. Musarò 2001 (Nat Genet) and the mIGF-1 transgenic line reproduced the hypertrophy in mice without elevating circulating IGF-1. These are the foundational animal studies cited by off-label users — they demonstrate local mechanism but do not translate to a published human RCT of systemic IGF-1 for healthy-adult muscle mass.

  5. 05

    IGFBP regulation and why free IGF-1 is rare

    In serum, 70–80% of IGF-1 circulates in a 150-kDa ternary complex with IGFBP-3 and the acid-labile subunit (ALS), extending half-life from ~5 minutes (free) to ~20 hours (bound). About 20% is in 50-kDa binary complexes with the other five IGFBPs. Less than 5% is free. Proteolytic cleavage of IGFBPs by PAPP-A and related proteases liberates IGF-1 locally. The mecasermin rinfabate formulation (IGF-1 + IGFBP-3 co-administered) was designed to exploit this — but was discontinued. IGF-1 LR3's clinical logic in research-chemical channels is that its reduced IGFBP binding raises free IGF-1 — which is precisely why its safety margin is narrower than native IGF-1.

  6. 06

    What is NOT known about the mechanism in off-label use

    Tissue-specific signaling bias of systemic IGF-1 in healthy adults is not characterized. Chronic-dosing feedback (mTORC1 → S6K → IRS-1 degradation, generating insulin resistance; Copps & White 2012) is documented but its magnitude and reversibility at off-label doses are not published. The downstream proliferative consequence across tissues — particularly on prostate epithelium, colonic mucosa, and breast tissue, the three sites with the strongest Renehan 2004 meta-analysis signal — is the central safety question that off-label dosing regimens have not answered.

§ Investigated uses

What it’s
been studied for.

Investigated does not mean proven. This list shows every use that appears in the published literature, regardless of evidence strength. See the grade matrix above for which ones have actually held up.

  • Severe primary IGF-1 deficiency (pediatric, SDS ≤ −3 with normal GH)

    FDA-approved 2005 as mecasermin (Increlex). Chernausek 2007, Backeljauw 2013 open-label extension over 8 years

  • GH gene deletion with neutralizing anti-GH antibodies

    FDA-approved as mecasermin

  • Severe type A and type B insulin resistance syndromes

    Small open-label series; reviewed Clemmons 2007. Not a broad-population therapy

  • Type 1 and type 2 diabetes (adjunct for glycemic control)

    Phase II mecasermin rinfabate (IGF-1/IGFBP-3) trials in adults; program not advanced to Phase 3

  • ALS (amyotrophic lateral sclerosis)

    Two RCTs (Lai 1997 positive; Sorenson 2008 null, n=330). Not indicated

  • Moderate-to-severe traumatic brain injury

    Hatton 2006 Phase II — nitrogen retention but no functional benefit

  • Muscle hypertrophy and strength in healthy adults

    Animal models only (Barton-Davis 1998; Musarò 2001). No published human RCT of systemic IGF-1 for this endpoint

  • Anti-aging / longevity

    Contra-indicated by model-organism lifespan data and Laron-syndrome human cohort (Guevara-Aguirre 2011)

  • Sarcopenia in older adults

    Observational only. U-shaped risk curve in NHANES III (Friedrich 2012)

  • Rett syndrome (neurodevelopmental)

    Small open-label trials of mecasermin (Khwaja 2014, Glaze 2019); mixed signal, no Phase 3 efficacy

§ The honest gaps

What we don’t
know yet.

Every peptide page on this site is required to include this section. Absence of evidence is information. If we don’t flag the gaps, we’re lying by omission.

  • !

    No randomized placebo-controlled trial of systemic IGF-1 or IGF-1 LR3 has demonstrated efficacy for muscle hypertrophy, strength, or body composition in healthy adults. The common off-label use case is unsupported by controlled human evidence.

  • !

    Long-term cancer risk of chronic exogenous IGF-1 in healthy adults is not characterized. The Renehan 2004 prospective-cohort meta-analysis links endogenous circulating IGF-1 to colorectal, breast, and prostate cancer; no trial has been powered to quantify risk from exogenous dosing.

  • !

    Human pharmacokinetics of IGF-1 LR3 are essentially absent from peer-reviewed literature. Research-chemical LR3 users rely on mecasermin-label PK that does not apply to the LR3 analog.

  • !

    Optimal dose and duration for any off-label use is not defined. The Increlex label (0.04–0.12 mg/kg twice daily, titrated) applies only to pediatric severe IGFD with endocrinologist supervision.

  • !

    Interaction with endogenous GH/IGF-1 axis under chronic exogenous dosing is not characterized — specifically whether long-term exogenous IGF-1 suppresses pituitary GH and shifts the balance of free vs IGFBP-bound IGF-1.

  • !

    Durable neuroprotection in adult humans after TBI or stroke has not been demonstrated despite a strong animal signal. Song 2016 documented that sustained Akt–mTOR activation by IGF-1 was pro-epileptic in rodents — a concerning translational counterweight.

  • !

    Immunogenicity with chronic subcutaneous dosing is partially characterized in the Increlex pediatric cohort but not in adults, and not for the LR3 analog.

  • !

    Real-world purity and identity of IGF-1 LR3 sold as research chemical is unverified. No cGMP requirement, no required certificate of analysis, no mass-spec or HPLC guarantee unless the supplier elects to publish it.

§ On YouTube

What experts and
influencers say.

We index YouTube content discussing IGF-1and tag every speaker by credential and trust level. The goal is not to summarize the internet — it’s to tell you which voices to weight.

  • The IGF-1 Paradox — Growth Factor vs Longevity Signal

    Peter Attia MD·MD, Longevity Medicine

    Walks through the Renehan meta-analysis and Laron cohort data. Explicit that the same signaling that drives hypertrophy drives proliferation, and that chronic elevation in healthy adults is directionally opposite to a longevity strategy.

    Verified credentials

  • Mecasermin (Increlex) in Clinical Endocrinology — When IGF-1 Therapy is Actually Indicated

    Dr. Kyle Gillett·MD, Family Medicine

    Covers the narrow pediatric severe-primary-IGFD approval, the boxed warning set, and why the off-label adult muscle-growth use case does not map to the approved dosing paradigm.

    Verified credentials

  • IGF-1 LR3 for Muscle Growth — My 8-Week Cycle Results

    Anonymous bodybuilding channel·Unverified

    Typical off-label-use content: anecdotal muscle-mass claims, no objective measurement, no discussion of cancer signal, no awareness that LR3 has no human PK data. Common pattern in research-chemical content. Do not weight against published evidence.

    Caution — anecdotal

§ Citations

Every claim,
linked to source.

All 18 sources informing this page, with DOI or PubMed identifiers. Click through to the primary literature.

  1. [01]

    Long-term treatment with recombinant insulin-like growth factor (IGF)-I in children with severe IGF-I deficiency due to growth hormone insensitivity

    Chernausek SD, Backeljauw PF, Frane J, Kuntze J, Underwood LE · J Clin Endocrinol Metab · 2007

    Open-labelPMID 17595246
  2. [02]

    Effect of 8 years of long-term recombinant IGF-1 therapy on growth in children with severe primary IGF-1 deficiency

    Backeljauw PF, Kuntze J, Frane J, Calikoglu AS, Chernausek SD · Horm Res Paediatr · 2013

    Open-labelPMID 23543660
  3. [03]

    Viral mediated expression of insulin-like growth factor I blocks the aging-related loss of skeletal muscle function

    Barton-Davis ER, Shoturma DI, Musarò A, Rosenthal N, Sweeney HL · Proc Natl Acad Sci USA · 1998

    AnimalPMID 9207156
  4. [04]

    Mediation of IGF-1-induced skeletal myotube hypertrophy by PI(3)K/Akt/mTOR and PI(3)K/Akt/GSK3 pathways

    Rommel C, Bodine SC, Clarke BA, et al. · Nat Cell Biol · 2001

    In vitroPMID 11715022
  5. [05]

    Subcutaneous IGF-1 is not beneficial in 2-year ALS trial

    Sorenson EJ, Windbank AJ, Mandrekar JN, et al. · Neurology · 2008

    RCTPMID 18525028
  6. [06]

    Effect of recombinant human insulin-like growth factor-I on progression of ALS: a placebo-controlled study

    Lai EC, Felice KJ, Festoff BW, et al. · Neurology · 1997

    RCTPMID 9339705
  7. [07]

    Insulin-like growth factor-I and cancer risk: a systematic review and meta-analysis

    Renehan AG, Zwahlen M, Minder C, O'Dwyer ST, Shalet SM, Egger M · Lancet · 2004

    Meta-analysisPMID 15126391
  8. [08]

    Growth hormone receptor deficiency is associated with a major reduction in pro-aging signaling, cancer, and diabetes in humans

    Guevara-Aguirre J, Balasubramanian P, Guevara-Aguirre M, et al. · Sci Transl Med · 2011

    CohortPMID 21325617
  9. [09]

    Intravenous insulin-like growth factor-I and insulin-like growth factor binding protein-3 for traumatic brain injury

    Hatton J, Rapp RP, Kudsk KA, et al. · J Neurosurg · 2006

    RCTPMID 16636319
  10. [10]

    Metabolic actions of insulin-like growth factor-I in normal physiology and diabetes

    Clemmons DR · Endocrinol Metab Clin North Am · 2012

    Systematic reviewPMID 17299449
  11. [11]

    The first long-lived mutants: discovery of the insulin/IGF-1 pathway for ageing

    Kenyon CJ · Philos Trans R Soc Lond B Biol Sci · 2011

    Systematic reviewPMID 20392241
  12. [12]

    IGF1 receptor signaling pathways

    Hakuno F, Takahashi SI · J Mol Endocrinol · 2018

    Systematic reviewPMID 29686378
  13. [13]

    Foxo transcription factors induce the atrophy-related ubiquitin ligase atrogin-1 and cause skeletal muscle atrophy

    Sandri M, Sandri C, Gilbert A, et al. · Cell · 2004

    In vitroPMID 15531763
  14. [14]

    Safety, pharmacokinetics, and preliminary assessment of efficacy of mecasermin (recombinant human IGF-1) for the treatment of Rett syndrome

    Khwaja OS, Ho E, Barnes KV, et al. · Proc Natl Acad Sci USA · 2014

    Open-labelPMID 24739126
  15. [15]

    Low serum insulin-like growth factor I is associated with increased risk of ischemic stroke (U-shaped association)

    Friedrich N, Thuesen B, Jørgensen T, et al. · J Clin Endocrinol Metab · 2012

    CohortPMID 22523333
  16. [16]

    Long-term effects of IGF-1 treatment are context-dependent and include pro-epileptic activity mediated by Akt-mTOR signaling

    Song Y, Pimentel C, Walters K, et al. · Sci Rep · 2016

    AnimalPMID 27558817
  17. [17]

    INCRELEX (mecasermin) injection, for subcutaneous use — US Prescribing Information with boxed warning for intracranial hypertension and lymphoid hypertrophy

    U.S. Food and Drug Administration / Ipsen Biopharmaceuticals · FDA · 2024

    RegulatoryLink
  18. [18]

    WADA 2026 Prohibited List — Section S2 Peptide Hormones, Growth Factors, Related Substances and Mimetics (IGF-1 and its analogs including LR3)

    World Anti-Doping Agency · WADA · 2026

    RegulatoryLink

§ Adjacent peptides

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alongside this.

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CJC-1295

GHRH analog that raises endogenous GH and downstream IGF-1. Users comparing exogenous IGF-1 to upstream GH-axis stimulation should read both pages.

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Ipamorelin

Cleanest GH secretagogue with documented human PK/PD. The indirect route to raising IGF-1 via endogenous GH pulse, with a different risk profile than exogenous IGF-1.

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Tirzepatide

Contrast case — an FDA-approved peptide hormone (GIP/GLP-1) for type 2 diabetes and obesity with a robust Phase 3 evidence base, versus IGF-1's narrow rare-disease approval.

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Semaglutide

Another FDA-approved therapeutic peptide. Useful comparator for what a high-evidence peptide-hormone program looks like against IGF-1's single approved indication.

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BPC-157

BPC-157 mechanism includes GH-receptor upregulation (Lovric-Bencic 2018). The tissue-repair mechanism overlaps with IGF-1 pathway modulation, though the evidence bases are very different.

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TB-500 (Thymosin β-4)

Frequently stacked with IGF-1 LR3 in off-label recovery protocols. Similar evidence pattern: strong preclinical, no human RCT, WADA-prohibited.

Read its grades

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Retatrutide

Triple-agonist investigational metabolic peptide — contrasts with IGF-1's narrow approval and illustrates what a modern Phase 3 metabolic program produces.

Read its grades

Where to research further

Looking for IGF-1
for laboratory research?

Peptigrade does not sell peptides. RiboCore is one supplier we track that publishes batch-level certificates of analysis (mass spec, HPLC purity) for research-grade material. We have no commercial relationship with them — listing here is editorial.

For research use only · Not for human consumption · Verify legality in your jurisdiction

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