IGF-1 LR3
Growth Hormone / IGF-1 AxisPhase 2Also known as: IGF-1 Long R3
IGF-1 LR3 (Long R3 IGF-1) is a synthetic analog of human insulin-like growth factor 1 modified at two positions to dramatically extend its serum half-life and amplify its tissue bioactivity compared to native IGF-1. The "LR3" designation describes the two key modifications: "L" (Long): A 13-amino-acid N-terminal extension peptide added to the native 70-amino-acid IGF-1 sequence "R3": An arginine substitution at position 3 (replacing the native glutamic acid) Together these modifications produce a critical pharmacologic consequence: dramatically reduced binding affinity for the insulin-like growth factor binding proteins (IGFBPs), particularly IGFBP-3 which normally sequesters 95-99% of circulating IGF-1 in an inactive reservoir.
Overview
At A Glance
IGF-1 Receptor Signaling…
Mechanism of Action
IGF-1 Receptor Signaling
IGF-1 LR3 binds the IGF-1 receptor (IGF1R) — a transmembrane receptor tyrosine kinase expressed on virtually every cell type in the human body. IGF1R activation triggers two principal intracellular signaling cascades:
PI3K / Akt / mTOR Pathway (the primary anabolic pathway):
- IGF1R autophosphorylation on ligand binding
- Recruitment and activation of IRS-1/2 adapter proteins
- Activation of phosphatidylinositol 3-kinase (PI3K)
- Akt phosphorylation
- mTORC1 activation → ribosomal S6K1 and 4E-BP1 phosphorylation
- Increased muscle protein synthesis, satellite cell proliferation, muscle fiber hypertrophy
Ras / MAPK Pathway (proliferation and differentiation):
- IGF1R-mediated Ras activation
- Raf → MEK → ERK cascade
- Nuclear translocation of activated ERK
- Transcription factor phosphorylation (c-Myc, c-Fos, others)
- Cell cycle progression, proliferation, differentiation
The combination of strong mTOR activation and moderate proliferative signaling is what drives the dramatic muscle-building effects of IGF-1 LR3 when used at anabolic doses — but also what underlies the theoretical cancer-promotion concern and the peripheral tissue growth issues (gut hypertrophy, organ enlargement with chronic high-dose use).
Why IGFBP Binding Matters
Native IGF-1 circulates in serum at ~150-300 ng/mL, but 95-99% is bound to IGFBP-3 (primarily) and IGFBPs 1, 2, 4, 5, 6. This bound form is:
- Biologically inactive — cannot bind IGF1R in the bound state
- Long-lived — 12-15 hour complex half-life, providing a reservoir
- Released slowly — IGFBP proteases (PAPP-A, others) cleave IGFBP-3 to release free IGF-1 in controlled, tissue-specific fashion
This IGFBP buffer system is fundamentally important to IGF-1 physiology — it is what prevents the mitogenic/hypoglycemic risks of free IGF-1 while maintaining a steady tissue supply. The LR3 modifications bypass this buffer:
| Parameter | Native IGF-1 | IGF-1 LR3 |
|---|---|---|
| IGFBP-3 binding affinity | High | ~60% reduced |
| IGFBP-1 binding affinity | High | Essentially abolished |
| Free fraction in serum | ~1-2% | ~10-30% |
| Serum half-life | ~12 minutes | 20-30 hours |
| Tissue bioactivity | Regulated | Supraphysiologic |
The practical implication: a small dose of IGF-1 LR3 produces disproportionately large biological effects compared to native IGF-1. This is the therapeutic benefit and the risk in one property.
Insulin Receptor Cross-Reactivity
IGF-1 LR3 binds the insulin receptor (InsR) with modest affinity — on the order of 1-10% of its IGF1R affinity. This cross-reactivity is pharmacologically significant because insulin receptor activation drives glucose uptake into muscle and adipose tissue:
- Post-injection hypoglycemia risk in users who dose without appropriate carbohydrate intake
- Enhanced glucose disposal during and after resistance training
- Additive hypoglycemia risk when combined with exogenous insulin, sulfonylureas, or aggressive carbohydrate restriction
Hypoglycemia is the primary acute safety concern with IGF-1 LR3. Users must plan carbohydrate intake around dosing — specifically, 30-40g of fast-digesting carbohydrate within 30 minutes of injection is the conservative recommendation.
Tissue-Wide Receptor Expression (The Peripheral Growth Problem)
Unlike the pituitary GH-axis, where GHRH and GHS receptors are concentrated on somatotrophs, the IGF-1 receptor is ubiquitous — expressed on:
- Skeletal muscle (the intended target)
- Intestinal epithelium (drives gut hypertrophy with chronic high doses)
- Liver, spleen, kidneys (organ enlargement)
- Cardiac myocardium (cardiac hypertrophy — generally not desired)
- Smooth muscle
- Bone
- Skin and connective tissue
- Various cancer cell types (mechanistic concern)
At high cumulative doses used by bodybuilders (50+ mcg/day for weeks), peripheral growth effects are real and measurable — particularly a distinctive "IGF gut" appearance from intestinal hypertrophy that characterizes aggressive IGF-1 LR3 users.
Half-Life and Kinetics
The 20-30 hour half-life allows once-daily dosing. Peak serum concentrations occur 2-6 hours post-SC injection, with sustained elevation for 24+ hours. This pharmacology is distinct from native IGF-1 (12 min half-life, would require continuous infusion) and is what makes LR3 practically usable in outpatient contexts.
Overview
IGF-1 LR3 (Long R3 IGF-1) is a synthetic analog of human insulin-like growth factor 1 modified at two positions to dramatically extend its serum half-life and amplify its tissue bioactivity compared to native IGF-1. The "LR3" designation describes the two key modifications:
- "L" (Long): A 13-amino-acid N-terminal extension peptide added to the native 70-amino-acid IGF-1 sequence
- "R3": An arginine substitution at position 3 (replacing the native glutamic acid)
Together these modifications produce a critical pharmacologic consequence: dramatically reduced binding affinity for the insulin-like growth factor binding proteins (IGFBPs), particularly IGFBP-3 which normally sequesters 95-99% of circulating IGF-1 in an inactive reservoir. Free (unbound) IGF-1 is the bioactive form that binds the IGF-1 receptor and drives muscle protein synthesis. By escaping IGFBP sequestration, IGF-1 LR3 produces:
- Serum half-life of 20-30 hours (native IGF-1: ~12 minutes)
- 3-10 times higher bioactive concentration in target tissues
- Stronger and more sustained IGF-1 receptor signaling per dose
IGF-1 LR3 was originally developed by Francis et al. in the early 1990s at CSIRO Australia for cell culture applications — specifically, driving growth of mammalian cell lines in bioreactors where the IGFBPs from fetal bovine serum would otherwise neutralize added growth factor. This commercial research-chemical origin is the reason IGF-1 LR3 has been widely available in the research-peptide supply chain for decades despite never pursuing a clinical drug approval pathway.
There is no FDA-approved indication for IGF-1 LR3 in human use. Mecasermin (recombinant native human IGF-1, Increlex) is FDA-approved for severe primary IGF-1 deficiency in children but is mechanistically very different — it is native IGF-1 with normal IGFBP binding and a short half-life.
Off-label and research-chemical use of IGF-1 LR3 is concentrated in the bodybuilding and athletic performance community, typically at doses of 20-60 mcg SC once daily or post-workout. It is one of the most potent anabolic peptides available but also one of the highest-risk due to hypoglycemia (cross-reactivity at the insulin receptor), unintended peripheral tissue growth (IGF-1R is expressed on virtually every tissue in the body including the intestine, organs, and connective tissue), and theoretical cancer-promotion risk from sustained supraphysiologic mitogenic signaling. Users who choose IGF-1 LR3 should understand the risk profile differs fundamentally from GHRH/GHS peptides that work through the body's native pituitary axis.
Potential Research Fields
Chemical Information
IUPAC Name
Insulin-like growth factor I, 7-70-peptide (synthetic) 1-[(2S)-2-amino-2-carboxyethyl] compound
CAS Number
946870-92-4
Molecular Formula
C400H625N111O115S9
Molecular Mass
9117.6 g/mol
Dosing & Protocols
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Interactions
Interaction Matrix
Contraindications
IGF-1 LR3 is contraindicated or requires strict caution in:
Absolute contraindications:
- Active malignancy, any type — IGF-1 is a pro-mitogenic signal; IGF1R is expressed on virtually all cancer cells; supraphysiologic IGF-1 exposure in the presence of malignant cells has mechanistic cancer-promotion risk
- Strong family history of breast, prostate, colon, or other hormonally-responsive cancers — elevated IGF-1 is an epidemiologic risk factor for these cancers
- Active proliferative retinopathy — IGF-1 drives retinal neovascularization
- Pregnancy and lactation — no safety data; theoretical fetal growth effects
- Pediatric or adolescent use without specialist supervision — growth plate and organ development concerns
- Hypoglycemia unawareness or severe hypoglycemic episodes in history — acute safety risk is unacceptable
- Known hypersensitivity to IGF-1 LR3 or IGF-1 analogs
Strong relative cautions:
- Diabetes mellitus (any type) — hypoglycemia risk is significantly elevated and the condition itself involves disrupted IGF-1/insulin signaling
- Prior history of any cancer, even if treated and disease-free — specialist supervision required if used at all
- Active or treated pituitary adenoma — IGF-1 axis disruption concerns
- Organomegaly (hepatomegaly, splenomegaly) — will worsen
- Active intestinal disease (Crohn's, ulcerative colitis, severe diverticular disease) — gut growth effects may worsen symptoms
- Severe cardiovascular disease — cardiac hypertrophy concerns
- Sleep apnea (untreated) — soft-tissue growth may worsen airway obstruction
Relative cautions (monitor closely):
- Borderline glucose tolerance or HbA1c
- Any history of benign tumor/adenoma (pituitary, adrenal, parathyroid)
- Strong family history of colon polyps — colonoscopy surveillance essential
- Users on immunosuppressants — theoretical concern about IGF-1 effects on cancer surveillance
- Users with low-grade chronic inflammation or elevated hs-CRP — IGF-1 may modulate inflammation in complex ways
- Users with prior skin cancer (even non-melanoma) — dermatology surveillance required
Drug interactions (dangerous):
- Insulin (exogenous): Compounded hypoglycemia; potentially life-threatening combination
- Sulfonylureas (glipizide, glyburide): Compounded hypoglycemia
- Meglitinides (repaglinide): Compounded hypoglycemia
- Mecasermin (Increlex): Redundant; both IGF1R agonists; excessive IGF1R activation
Drug interactions (manage):
- Corticosteroids (high-dose prednisone, dexamethasone): Pharmacodynamic antagonism
- Aromatase inhibitors (letrozole, anastrozole): May modify IGF-1 signaling indirectly
- Statins: Some evidence of IGF-1 effects modulation
- Thyroid hormone: Thyroid status affects IGF-1 receptor sensitivity
Discontinuation triggers (immediate):
- Any new or growing skin lesion, mass, or lymphadenopathy
- Unexplained weight loss
- Symptomatic abdominal distension, early satiety, or imaging abnormality
- Persistent fasting glucose >110 mg/dL despite appropriate carb management
- New chest pain, shortness of breath, or other cardiovascular symptoms
- Facial or extremity changes suggesting acromegalic growth
- Any severe hypoglycemic episode despite appropriate carb intake
- Strong family cancer history revealed after starting use
Research Disclaimer
This interaction data is compiled from published research and community reports. It may not be exhaustive. Always consult a healthcare professional before combining compounds.
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Related Compounds
View AllCJC-1295 (Mod GRF 1-29)
Growth Hormone / IGF-1 AxisPreclinicalCJC-1295 without DAC (also called Modified GRF 1-29 or MOD-GRF 1-29) is a 30-amino-acid analog of the first 29 residues of endogenous Growth Hormone Releasing Hormone (GHRH), with four strategic substitutions (D-Ala² for DPP-4 resistance, Gln⁸, Ala¹⁵, Leu²⁷) that extend its plasma half-life from <2 minutes (native GHRH) to ~30 minutes.
CJC-1295 with DAC
Growth Hormone / IGF-1 AxisPhase 2CJC-1295 with DAC (Drug Affinity Complex) is a modified form of CJC-1295 that incorporates a maleimidopropionic acid (MPA) reactive group at the C-terminus.
GHRP-2
Growth Hormone / IGF-1 AxisPhase 2GHRP-2 (growth hormone-releasing peptide-2), also known as pralmorelin and KP-102, is a synthetic hexapeptide growth hormone secretagogue that was among the first GHRPs developed in the seminal research of Cyril Bowers and colleagues at Tulane University in the late 1980s and early 1990s.
GHRP-6
Growth Hormone / IGF-1 AxisPhase 2GHRP-6 (growth hormone-releasing peptide-6) is a synthetic hexapeptide with the sequence His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 that binds the ghrelin receptor (GHS-R1a) to stimulate endogenous growth hormone release.
Hexarelin
Growth Hormone / IGF-1 AxisPhase 2Hexarelin (also called examorelin) is a potent synthetic hexapeptide growth hormone secretagogue with the sequence His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH2.
Ipamorelin
Growth Hormone / IGF-1 AxisPreclinicalIpamorelin is a selective pentapeptide ghrelin receptor (GHS-R1a) agonist — one of the most studied growth hormone secretagogues (GHS) in the biohacking community and the modern companion to CJC-1295 / MOD-GRF 1-29.
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Protocols, calculator & safety for IGF-1 LR3
Research Score
40 PubMed studies
Quality Indicators
Data Completeness
100%COA Verification
10
Verified COAs
2
Vendors w/ COA
High verification rate (83%)
Latest test: 3/1/2026
Research Credibility
Quick Facts
Half-Life
20–30 hours (vs 12–15 minutes for native IGF-1)
Molecular Weight
9117.6 g/mol
Administration
Subcutaneous, Intramuscular
CAS Number
946870-92-4
Trial Phase
Phase 2
Safety Profile
Moderate RiskCommon Side Effects
- • Hypoglycemia (dose-dependent)
- • Jaw pain
- • Headache
- • Fatigue
Stop Use If
- Active malignancy — IGF-1 is mitogenic
- Diabetic retinopathy
- Severe hypoglycemia episodes
Research Disclaimer
This information is for educational and research purposes only. Not intended as medical advice. Consult a healthcare professional before use.
Frequently Asked Questions
What is IGF-1 LR3 and how does it work?
IGF-1 LR3 (Long R3 IGF-1) is a synthetic analog of human insulin-like growth factor 1 modified with a 13-amino-acid N-terminal extension and an arginine-for-glutamic-acid substitution at position 3. These modifications dramatically reduce its binding to IGFBP-3 (the main serum carrier protein for IGF-1), producing an IGF-1 molecule that circulates in the free/active form rather than bound/inactive form. Result: serum half-life of 20-30 hours (vs 12 min for native IGF-1), 3-10x higher bioactive tissue concentration, and strong sustained IGF-1 receptor signaling. It's used off-label by bodybuilders and athletes to drive muscle protein synthesis via PI3K/Akt/mTOR pathway activation. It is not FDA-approved for any indication; research-chemical use only.
How is IGF-1 LR3 different from HGH?
HGH (human growth hormone) is an upstream signal — it travels to the liver where it stimulates IGF-1 production, which then mediates most of HGH's anabolic effects. IGF-1 LR3 bypasses this pathway and directly provides the downstream effector molecule in a long-acting form. Practical differences: HGH has additional effects beyond IGF-1 (direct lipolysis, insulin sensitivity changes, bone metabolism), while IGF-1 LR3 is purely an IGF1R agonist. HGH requires pituitary function; IGF-1 LR3 works regardless. HGH has a better safety profile at physiologic doses because the endogenous IGFBP system regulates IGF-1 availability; IGF-1 LR3 bypasses this safety mechanism and can produce supraphysiologic free IGF-1. For cleaner GH-axis support, use GHRH + GHS peptides that drive endogenous production. For raw IGF1R activation, IGF-1 LR3.
What is the best IGF-1 LR3 dosage?
Beginner dose is 20 mcg SC once daily for 4 weeks. Intermediate users progress to 30-50 mcg SC daily for 4-6 weeks. Advanced users run 50-80 mcg daily. ALWAYS dose with 30-40g of fast-digesting carbohydrate within 30 minutes to prevent hypoglycemia — this is the most important rule. Cycle 4-6 weeks on with 2-4 week washouts. Post-workout timing (with a carb/protein shake) is popular but morning-with-breakfast is safer for beginners. Do not exceed 8 consecutive weeks of use. Do not combine with exogenous insulin under any circumstances. Monitor fasting glucose weekly during first cycle and IGF-1 quarterly during long-term use.
Does IGF-1 LR3 cause hypoglycemia?
Yes — this is the primary acute safety concern. IGF-1 LR3 cross-reacts with the insulin receptor (at ~1-10% of its IGF1R affinity) and independently activates insulin-like glucose uptake into muscle and adipose tissue. Hypoglycemic episodes can produce shakiness, sweating, confusion, palpitations, and in severe cases loss of consciousness. Prevention: always dose with 30-40g fast-digesting carbohydrate within 30 minutes of injection. Never dose fasted. Never combine with exogenous insulin (can be life-threatening). Test blood glucose during first 3-5 doses. Have glucose tabs or juice readily available. Users in caloric deficit or on keto/low-carb diets should either abandon those approaches or choose a different anabolic peptide — IGF-1 LR3 is incompatible with aggressive carbohydrate restriction.
What is 'IGF gut' or peripheral tissue growth?
Chronic high-dose IGF-1 LR3 use drives growth of any tissue expressing the IGF-1 receptor — which is essentially every tissue in the body. The most visually distinctive effect is intestinal epithelial hypertrophy ('IGF gut'), producing an abdominal distension characteristic of aggressive bodybuilding IGF-1 users. At high cumulative doses (60-80+ mcg/day for multiple cycles), liver, spleen, kidneys, and occasionally cardiac muscle can also show measurable enlargement on imaging. Lymphoid tissue (tonsils, adenoids, lymph nodes) can also enlarge. These effects are generally reversible with discontinuation over weeks to months but illustrate a fundamental point: IGF-1 LR3 is a systemic anabolic agent, not a muscle-specific one. The same signal that grows muscle also grows every other IGF1R-expressing tissue. This is why cycling and dose conservatism matter.
Does IGF-1 LR3 cause cancer?
This is the most important long-term theoretical concern. IGF-1 is a potent pro-mitogenic signal; virtually every malignancy overexpresses the IGF-1 receptor; elevated IGF-1 is an epidemiologic risk factor for breast, prostate, and colon cancers in population studies. Sustained supraphysiologic IGF-1 LR3 signaling has mechanistic plausibility for promoting the growth of any pre-existing occult malignant cells, even if it does not cause cancer to arise in otherwise healthy tissue. No large-population longitudinal studies exist specifically for IGF-1 LR3 use; the safety profile is inferred from mecasermin pediatric data and short-term observations. Users should understand this is a real theoretical concern, approach dosing conservatively, cycle strictly, undergo regular cancer screening appropriate for age and family history, and avoid IGF-1 LR3 entirely if any pre-existing cancer risk factors apply.
Can IGF-1 LR3 be stacked with testosterone or anabolic steroids?
Yes — this is a classical bodybuilding stack. Testosterone drives muscle protein synthesis through androgen receptor signaling; IGF-1 LR3 through IGF1R/PI3K/mTOR. Additive hypertrophic effects. This combination is central to off-label performance use but carries combined risk: the cancer-promotion concerns of sustained IGF-1 elevation compound with the cancer concerns of testosterone or AAS use, the cardiac strain of both agents is additive, and the hepatic and metabolic effects stack. Done in specialist-supervised medical contexts with appropriate surveillance (labs, imaging, cancer screening), this combination has been used for decades. Done in unsupervised self-experimentation, the risk profile is substantial. For GH-axis support specifically, a cleaner alternative is stacking GHRH + GHS peptides that drive endogenous IGF-1 production at physiologic levels rather than supraphysiologic free IGF-1 via LR3.
How long does it take IGF-1 LR3 to work?
Subjective muscle fullness and pump effects are often noticed within the first 2-3 doses. Measurable strength gains typically appear at weeks 2-4 of consistent use. Lean mass changes become clearly detectable at weeks 4-6, with 2-5 kg gains in lean body mass during a 4-6 week cycle in experienced users who are training hard and eating in caloric surplus. Recovery effects (reduced soreness, faster workout-to-workout bounce-back) are usually noticed within the first week. Results vary substantially based on training intensity, caloric intake, protein intake, sleep quality, and whether the user is stacking with other anabolic agents. Some users notice very little effect; others see dramatic results. The variability reflects both individual biological differences and the wide variation in supporting protocols.
Is IGF-1 LR3 legal?
IGF-1 LR3 is not FDA-approved for any human use. It is sold through the research-chemical market under research-only classification. Native human IGF-1 (mecasermin, Increlex) is FDA-approved for severe primary IGF-1 deficiency in children — a distinct and tightly regulated medical use. Off-label IGF-1 LR3 use in the United States for performance or bodybuilding purposes is outside medical regulation. Users should understand this legal context, source from vendors with third-party purity testing, and ideally work with a practitioner experienced with off-label peptide therapy. Some 503B compounding pharmacies include IGF-1 analogs in their physician-supervised offerings, though LR3 specifically is less commonly compounded than mecasermin. See our best vendors guide for reliable research-peptide sources.
Should I use IGF-1 LR3 or MK-677?
They achieve similar end effects (elevated IGF-1) through fundamentally different pathways with different risk profiles. MK-677 is an oral GHS-R1a agonist that drives endogenous pituitary GH release, which then stimulates native hepatic IGF-1 production with normal IGFBP binding and regulation. Advantages: oral dosing, works through the native physiologic axis with intact safety systems, once-daily convenience, less peripheral tissue growth concern, better long-term safety profile. Disadvantages: less raw anabolic potency, more fluid retention, more appetite stimulation, more insulin resistance over time, requires pituitary function. IGF-1 LR3 is exogenous free IGF-1 that bypasses the IGFBP safety system. Advantages: more potent anabolic effect per dose, works regardless of pituitary function, more targeted IGF-1R activation. Disadvantages: hypoglycemia risk, peripheral tissue growth, unknown long-term safety, injection required, higher cancer-concern theoretical profile. For most users seeking GH-axis benefits with reasonable safety, MK-677 or GHRH+GHS peptide stacks are better choices. IGF-1 LR3 is reserved for aggressive anabolic contexts where the user has accepted the risk profile. See MK-677 for detailed comparison.
Research Tools
Related Compounds
View AllCJC-1295 (Mod GRF 1-29)
Growth Hormone / IGF-1 AxisPreclinicalCJC-1295 without DAC (also called Modified GRF 1-29 or MOD-GRF 1-29) is a 30-amino-acid analog of the first 29 residues of endogenous Growth Hormone Releasing Hormone (GHRH), with four strategic substitutions (D-Ala² for DPP-4 resistance, Gln⁸, Ala¹⁵, Leu²⁷) that extend its plasma half-life from <2 minutes (native GHRH) to ~30 minutes.
CJC-1295 with DAC
Growth Hormone / IGF-1 AxisPhase 2CJC-1295 with DAC (Drug Affinity Complex) is a modified form of CJC-1295 that incorporates a maleimidopropionic acid (MPA) reactive group at the C-terminus.
GHRP-2
Growth Hormone / IGF-1 AxisPhase 2GHRP-2 (growth hormone-releasing peptide-2), also known as pralmorelin and KP-102, is a synthetic hexapeptide growth hormone secretagogue that was among the first GHRPs developed in the seminal research of Cyril Bowers and colleagues at Tulane University in the late 1980s and early 1990s.
GHRP-6
Growth Hormone / IGF-1 AxisPhase 2GHRP-6 (growth hormone-releasing peptide-6) is a synthetic hexapeptide with the sequence His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 that binds the ghrelin receptor (GHS-R1a) to stimulate endogenous growth hormone release.
Hexarelin
Growth Hormone / IGF-1 AxisPhase 2Hexarelin (also called examorelin) is a potent synthetic hexapeptide growth hormone secretagogue with the sequence His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH2.
Ipamorelin
Growth Hormone / IGF-1 AxisPreclinicalIpamorelin is a selective pentapeptide ghrelin receptor (GHS-R1a) agonist — one of the most studied growth hormone secretagogues (GHS) in the biohacking community and the modern companion to CJC-1295 / MOD-GRF 1-29.
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