MEDICAL DISCLAIMER: Educational research guidelines only. Lyophilized peptides are investigational chemical compounds and are NOT approved for human consumption, diagnosis, or therapy. Consult a licensed physician before any research application.
IGF-1 DES Dosage Chart, Schedule & Reconstitution Protocol
Quickstart Highlights
IGF-1 DES (DES(1-3)IGF-1) is a 67-amino-acid truncated form of insulin-like growth factor-1, made by deleting the N-terminal Gly-Pro-Glu tripeptide from the natural 70-residue molecule [1]. That small change lets it largely bypass the IGF binding proteins that normally sequester about 99% of circulating IGF-1, so it acts as a nearly free, immediately available agonist at the type 1 IGF receptor (IGF-1R) and signals through PI3K/Akt/mTOR and Ras/MAPK to drive protein synthesis, glucose uptake and satellite-cell activity [2][7]. In IGFBP-rich systems it is roughly 10-fold more potent than native IGF-1 [1]. Unlike IGF-1 LR3, it has a very short half-life and is used for fast, localized IGF-1R activation near the injection site rather than sustained systemic exposure [2]. It is a research chemical with no FDA-approved indication and should not be confused with mecasermin (Increlex), the approved native IGF-1.
Reconstitute: Add 2 mL bacteriostatic water → 0.5 mg/mL concentration.
Typical dose: 20-100 mcg per injection (research)
Easy measuring: At 0.5 mg/mL, 1 unit = 0.01 mL = 0.0050 mg (5 mcg) on a U-100 insulin syringe.
Storage: Lyophilized powder frozen at −20 °C; reconstituted solution refrigerated at 2–8 °C and used within roughly 2–3 weeks; avoid repeated freeze–thaw cycles and direct light.
Half-life: Approximately 20-30 minutes. With little IGFBP buffering, the free peptide is cleared and proteolysed rapidly, giving fast, localized action rather than the multi-hour exposure of IGF-1 LR3 [2].
Route: Injected only (subcutaneous or local intramuscular). It is a peptide and is not orally active; the subcutaneous reconstitution figures are an injection reference, not an oral route.
Status: Not FDA or EMA approved; supplied strictly as a research chemical and prohibited in sport by WADA. Educational content only, not medical advice.
About IGF-1 DES
IGF-1 DES (DES(1-3)IGF-1) is a truncated form of insulin-like growth factor-1 missing the first three N-terminal amino acids, a change that lets the peptide largely escape capture by IGF binding proteins and act as an immediately available, high-potency IGF-1 receptor agonist[1][2]. Because it is not buffered in plasma by carrier proteins, it is cleared quickly and acts locally rather than systemically, which is the practical difference between IGF-1 DES and longer-acting analogues such as IGF-1 LR3[2].\n\nThis page models an educational subcutaneous reconstitution protocol. IGF-1 DES is a peptide and is not orally active (it would be digested if swallowed), so like native rhIGF-1 it is administered by injection; the subcutaneous and local intramuscular figures below are an injection reference, not an oral one. The most-discussed IGF-1 DES dosage in research and community settings is 20-100 mcg per injection on training days, frequently split bilaterally near the muscles being trained.\n\nFrequency: Inject on training days only (about 4 sessions per week), subcutaneously or locally near the worked muscle, typically post-workout with carbohydrate available because of the insulin-like glucose effect[7]. This protocol uses a 2.0 mL reconstitution so 20-100 mcg lands in a clean 4-20 unit range on a U-100 syringe. IGF-1 DES is a research chemical with no FDA or EMA approval; this is educational content, not medical advice.
Quick Protocol Navigation
Reconstitution Instruction & Mixing Step-by-Step
Lyophilized powder must be reconstituted carefully. Agitating peptide chains can shear disulfide bonds and render the peptide biologically inert.
Draw 2.0 mL of bacteriostatic water into a sterile syringe; this yields a 1 mg vial at 0.5 mg/mL (500 mcg/mL), so each U-100 unit equals 5 mcg.
Swab the vial stopper, then inject the water slowly down the inside wall of the vial rather than directly onto the powder to limit foaming; never shake.
Gently swirl or roll the vial until the lyophilized powder fully dissolves into a clear, colourless solution; discard if it stays cloudy or contains particulates.
Draw the target dose (e.g., 20 mcg = 4 units, 60 mcg = 12 units, 100 mcg = 20 units) and, if splitting bilaterally, divide between the two worked muscle areas.
Inject slowly and steadily into subcutaneous tissue or near the target muscle, hold for a few seconds before withdrawing to prevent leakage, then refrigerate the vial at 2-8 °C.
Interactive IGF-1 DES Syringe Calculator
Currently visualizing the 1 mg vial reconstituted with 2 mL bacteriostatic water. Adjust the target dose to dynamically render syringe units.
Reconstitution Calculation: 1mg dry powder in 2mL water yields 0.50 mg/mL. To evaluate a 250mcg dose, pull to 50.0 units (50 syringe ticks).
U-100 Syringe Representation
Educational reference visual. Assumes standard U-100 insulin syringe where 1.0 mL volume = 100 units.
Titration & Dose Escalation Schedules
| Phase | Dose per injection | Units (per injection) |
|---|---|---|
| Acclimation (Week 1) | 20 mcg | 4 units (0.04 mL) |
| Titration (Weeks 2-3) | 40 mcg | 8 units (0.08 mL) |
| Standard research (Weeks 4-6) | 60 mcg | 12 units (0.12 mL) |
| Upper community ceiling | 100 mcg | 20 units (0.20 mL) |
Administration guidelines: Refer to guidelines | 2 mL Reconstitution
Research Supplies Quantity Planner
Scientific mathematical planning of syringes, bacteriostatic water and dry vials needed for extended research blocks using the 1 mg vial.
Peptide Vials (IGF-1 DES, 1 mg each):
- check8 weeks ≈ 2 vials (~1.9 mg total at ~60 mcg × 4/week)
- check12 weeks ≈ 3 vials (~2.9 mg total)
- check16 weeks ≈ 4 vials (~3.8 mg total)
Insulin Syringes (U-100):
- checkPer week: 4 syringes (1 per training-day injection; double if splitting bilaterally into separate syringes)
- check8 weeks: 32 syringes
- check12 weeks: 48 syringes
- check16 weeks: 64 syringes
Bacteriostatic Water (10 mL bottles): Use 2 mL per vial for reconstitution.
- check8 weeks (2 vials): 4 mL → 1 × 10 mL bottle
- check12 weeks (3 vials): 6 mL → 1 × 10 mL bottle
- check16 weeks (4 vials): 8 mL → 1 × 10 mL bottle
Alcohol Swabs: One for the vial stopper plus one for each injection site.
- checkPer week: 8 swabs (2 per injection × 4 injections)
- check8 weeks: 64 swabs → 1 × 100-count box
- check12 weeks: 96 swabs → 1 × 100-count box
- check16 weeks: 128 swabs → 2 × 100-count boxes
Mechanism of Action (MOA)
IGF-1 DES, or DES(1-3)IGF-1, is a 67-amino-acid truncated analogue of insulin-like growth factor-1 produced by removing the N-terminal tripeptide glycine-proline-glutamate (Gly-Pro-Glu) from the 70-residue parent molecule[1]. It was first isolated from bovine colostrum and later identified in human fetal and adult brain tissue, so it is a naturally occurring IGF-1 fragment rather than a purely synthetic construct[1][2]. Despite the deletion it retains the disulfide-bonded tertiary fold needed to engage the type 1 IGF receptor (IGF-1R), a heterotetrameric receptor tyrosine kinase closely related to the insulin receptor. Ligand binding drives beta-subunit autophosphorylation, recruitment of IRS-1 and IRS-2, and activation of the PI3K-Akt-mTOR pathway that governs protein synthesis and cell survival, alongside Ras-MAPK signalling that mediates proliferation[7].\n\nThe defining feature of IGF-1 DES is its loss of affinity for the insulin-like growth factor binding proteins (IGFBP-1 through -6)[2]. Removal of Gly-Pro-Glu disrupts backbone contacts that native IGF-1 uses to dock into IGFBP-3 and related carriers, reducing IGFBP binding by roughly an order of magnitude (reported 10- to 70-fold depending on the binding protein and assay)[1][2]. Because about 99% of circulating native IGF-1 is sequestered by IGFBPs, a fragment that escapes this sequestration behaves as an almost entirely free, immediately available agonist. In IGFBP-rich systems it is roughly 10-fold more potent than IGF-1 at stimulating DNA and protein synthesis, and it retains a modest intrinsic advantage even in serum-free culture where IGFBPs are absent[1][5].\n\nPharmacokinetically, IGF-1 DES is the mirror image of long-acting analogues such as IGF-1 LR3. Without IGFBP carriage to buffer it in plasma, the free peptide is cleared and proteolysed rapidly, giving a very short circulating half-life on the order of 20-30 minutes[2]. In research and community settings it is therefore injected subcutaneously or locally (intramuscularly near a target muscle) rather than relied upon for sustained systemic exposure; the short half-life and rapid local clearance are used to concentrate IGF-1R activation near the injection site and limit systemic spillover. There is no oral route, because the peptide would be digested if swallowed, so the subcutaneous reconstitution figures here are an injection reference only.\n\nDownstream, IGF-1R activation increases amino-acid uptake, satellite-cell activity, glycogen storage and glucose uptake. Because IGF-1R shares high homology with the insulin receptor, IGF-1 DES retains insulin-like hypoglycaemic potential at higher doses[7]. Animal studies confirm anabolic, anti-catabolic and tissue-protective effects[3][4][5][6], but no human efficacy or safety trials exist; all use is research and educational only.
Clinical Trial Efficacy Highlights
- starFrancis et al. (Biochem J 1988) purified the truncated IGF-1 variant lacking Gly-Pro-Glu from bovine colostrum, established that its sequence matched human IGF-1 minus the N-terminal tripeptide, and showed it stimulated protein and DNA synthesis in cultured cells roughly 10-fold more potently than full-length IGF-1 [1].
- starBallard, Wallace, Francis, Read and Tomas (Int J Biochem Cell Biol 1996) reviewed DES(1-3)IGF-1 and attributed its enhanced potency to markedly reduced IGFBP binding combined with retained, even slightly increased, affinity for the IGF-1 receptor [2].
- starMartin, Tomas, Owens, Knowles, Ballard and Read (Am J Physiol 1991) gave des-(1-3)IGF-I at 0.9 mg/kg/day to rats with reduced renal mass and found significantly increased body-weight gain, food utilisation and nitrogen balance, partly via reduced muscle protein breakdown (lower 3-methylhistidine excretion) [3].
- starLemmey et al. (Am J Physiol 1991) showed that both IGF-I and the truncated analogue des-(1-3)IGF-I enhanced growth and gut recovery in rats after small-bowel resection, with the truncated form active at lower effective doses [4].
- starTomas et al. (Biochem J 1992) reported that in dexamethasone-treated (catabolic) rats, des-(1-3)IGF-I and LR3-IGF-I were about 2.5-fold more potent than native IGF-I at restoring nitrogen balance and limiting muscle protein loss [5].
- starKummer, Pulford, Ishii and Seigel (Int J Exp Diabesity Res 2003) found that Des(1-3)IGF-1 normalised type 1 IGF receptor and phospho-Akt (Thr308) immunoreactivity in the predegenerative retina of diabetic rats despite ongoing hyperglycaemia, supporting a direct neuroprotective IGF-1R mechanism [6].
- starNo human randomized controlled trials of IGF-1 DES exist; all human-relevant inference is extrapolated from rodent and cell models. For benchmarking, native rhIGF-1 (mecasermin, Increlex) is FDA-approved for severe primary IGF-1 deficiency, but IGF-1 DES is not a recognised therapeutic product [2].
Side Effects & Tolerability Profile
Clinical subjects transiently report mild side effects. Slowly escalating the titration dose represents the single most effective intervention to limit side effects.
- warningHypoglycaemia is the most predictable adverse effect and reflects IGF-1R cross-activation of insulin signalling; symptoms (sweating, tremor, light-headedness, palpitations) can appear within 1-2 hours and respond to oral carbohydrate. The short half-life tends to make episodes brief but does not eliminate them [7].
- warningInjection-site reactions, local pain, transient fullness or pump near the injected muscle, erythema and induration are commonly described in research-context use and reflect acute local IGF-1R activation and fluid uptake.
- warningTheoretical promotion of occult tumour growth is a serious concern because IGF-1R activation is mitogenic across many cell lines; chronic use is contraindicated in anyone with known or suspected malignancy [8].
- warningFrequent dosing can contribute to feedback suppression of endogenous growth hormone and IGF-1 secretion; the effect is generally smaller than with long-acting analogues because exposure is brief, but it is the rationale for limiting cycle length.
- warningFluid retention, peripheral oedema or joint and hand stiffness can occur through the same insulin-like and IGF-1R-mediated mechanisms seen with growth hormone, more likely with high or frequent dosing.
- warningLocal versus systemic targeting is imperfect; despite rapid clearance, some systemic spillover occurs, so site-specific effects should not be assumed to be confined to the injected muscle.
- warningProduct quality is a major real-world risk: research-grade IGF-1 DES is not manufactured to pharmaceutical standards, so purity, correct sequence, endotoxin and sterility are not guaranteed.
- warningThere are no human safety data and no FDA or EMA approval; IGF-1 DES is contraindicated in pregnancy, in children, and in anyone with active or prior cancer, and is for laboratory research use only.
Subcutaneous Injection Technique
Most research peptides require subcutaneous injection into fatty tissue. Never inject directly into a blood vessel or deep muscle tissue unless clinically detailed.
1. Site Selection
Common locations include the abdomen (2 inches from navel), outer upper arms, or thighs.
2. Sanitization
Thoroughly clean the selected site, stopper and vial top using 70% isopropyl alcohol prep swabs.
3. Angle & Push
Pinch the skin and insert the needle at a 45 to 90-degree angle. Depress plunger smoothly.
4. Site Rotation
Rotate injection sites continuously to avoid lipodystrophy or tissue scarring.
Frequently Asked Questions
What is the typical IGF-1 DES dosage?expand_more
In research and community references the typical IGF-1 DES dosage is 20-100 mcg per injection on training days, frequently split bilaterally near the muscles being worked. Many start at 20 mcg to gauge response and the glucose effect, then titrate toward 50-100 mcg. Because the half-life is short, it is dosed close to the training stimulus rather than once daily. These are not clinically validated doses; IGF-1 DES is a research chemical with no approved human dosing.
What is the IGF-1 DES half life?expand_more
IGF-1 DES has a very short circulating half-life of roughly 20-30 minutes. Native IGF-1 is buffered in plasma by IGF binding proteins, but because IGF-1 DES largely escapes those carriers it is cleared and degraded quickly. This is why it is treated as a fast, locally acting agent rather than a sustained systemic one like IGF-1 LR3, whose half-life is measured in hours to days.
How do you reconstitute IGF-1 DES?expand_more
Draw 2.0 mL of bacteriostatic water into a sterile syringe and add it slowly down the wall of a 1 mg vial, never directly onto the powder, then swirl gently until clear. This gives 0.5 mg/mL, so 1 U-100 unit equals 5 mcg: 20 mcg is 4 units, 60 mcg is 12 units and 100 mcg is 20 units. Store the reconstituted vial refrigerated at 2-8 °C and use it within about 2-3 weeks; do not shake or freeze-thaw.
How is IGF-1 DES different from IGF-1 LR3?expand_more
Both are IGF-1 receptor agonists engineered to evade IGF binding proteins, but they behave oppositely in time. IGF-1 LR3 has an arginine-3 substitution plus a 13-residue N-terminal extension that give it a 20-30 hour half-life for sustained systemic action. IGF-1 DES instead removes the first three amino acids, giving a 20-30 minute half-life and a fast, more localized, high-potency action near the injection site.
Is IGF-1 DES FDA approved?expand_more
No. IGF-1 DES (DES(1-3)IGF-1) is not approved by the FDA or EMA for any indication and is supplied solely as a research chemical. Only native rhIGF-1 (mecasermin, Increlex) is FDA-approved, and that is for severe primary IGF-1 deficiency, not for the muscle or performance uses associated with IGF-1 DES. IGF-1 and its analogues are also prohibited in sport by WADA. All information here is educational, not medical advice.
Related Guides & Tools
Step-by-step references for reconstituting, measuring, and storing IGF-1 DES, plus the universal dosing calculator.
Academic References & Study Citations
Francis GL, Upton FM, Ballard FJ, McNeil KA, Wallace JC. Insulin-like growth factors 1 and 2 in bovine colostrum. Sequences and biological activities compared with those of a potent truncated form. Biochem J. 1988;251(1):95-103. PMID: 3390164. View Scientific Paper →
Ballard FJ, Wallace JC, Francis GL, Read LC, Tomas FM. Des(1-3)IGF-I: a truncated form of insulin-like growth factor-I. Int J Biochem Cell Biol. 1996;28(10):1085-1087. PMID: 8930132. View Scientific Paper →
Martin AA, Tomas FM, Owens PC, Knowles SE, Ballard FJ, Read LC. IGF-I and its variant, des-(1-3)IGF-I, enhance growth in rats with reduced renal mass. Am J Physiol. 1991;261(4 Pt 2):F626-633. PMID: 1928375. View Scientific Paper →
Lemmey AB, Martin AA, Read LC, Tomas FM, Owens PC, Ballard FJ. IGF-I and the truncated analogue des-(1-3)IGF-I enhance growth in rats after gut resection. Am J Physiol. 1991;260(2 Pt 1):E213-E219. PMID: 1996625. View Scientific Paper →
Tomas FM, Knowles SE, Owens PC, Chandler CS, Francis GL, Read LC, Ballard FJ. Insulin-like growth factor-I (IGF-I) and especially IGF-I variants are anabolic in dexamethasone-treated rats. Biochem J. 1992;282(Pt 1):91-97. PMID: 1371669. View Scientific Paper →
Kummer A, Pulford BE, Ishii DN, Seigel GM. Des(1-3)IGF-1 treatment normalizes type 1 IGF receptor and phospho-Akt (Thr 308) immunoreactivity in predegenerative retina of diabetic rats. Int J Exp Diabesity Res. 2003;4(1):45-57. PMID: 12745670. View Scientific Paper →
LeRoith D, Yakar S. Mechanisms of disease: metabolic effects of growth hormone and insulin-like growth factor 1. Nat Clin Pract Endocrinol Metab. 2007;3(3):302-310. PMID: 17315038. View Scientific Paper →
Pollak M. The insulin and insulin-like growth factor receptor family in neoplasia: an update. Nat Rev Cancer. 2012;12(3):159-169. PMID: 22337149. View Scientific Paper →