IGF-1 with its first three amino acids removed, so binding proteins barely hold it. Studied in rats and cells; no human studies of any kind.
Also called Des(1-3)IGF-1, Des(1-3)IGF-I, Des1-3 IGF-I, DES IGF-1, Truncated IGF-1, IGF-1 DES 1-3
When IGF-1 DES's status or evidence changes, it's in the next morning's email.
IGF-1 DES, written des(1-3)IGF-I in research papers, is insulin-like growth factor 1 missing its first three amino acids, glycine, proline and glutamic acid. That leaves 67 of IGF-1's 70 amino acids. It occurs naturally in small amounts: it has been isolated from cow colostrum, human brain and pig uterus, probably cut from IGF-1 after it is made. Losing the glutamic acid at position 3 means the IGF binding proteins that normally hold most IGF-1 in the blood barely grip it, so more of it is free to reach the IGF-1 receptor.
In cultured cells it is generally about 10 times more potent than IGF-1. In rats it was 2.5 to 3 times more potent at restoring growth in diabetic rats, improved nitrogen balance after gut and kidney surgery, and had its strongest effects on the gut. It also cleared from rat blood almost 4 times faster than IGF-1. It is the same idea as IGF-1 LR3, which reaches the same result with an arginine swap and an extra 13-amino-acid tail instead of a deletion.
No human trial, pharmacokinetic study or safety study of IGF-1 DES has been published, and it was never developed as a drug. What is known about IGF-1 in humans comes from mecasermin (Increlex), recombinant native IGF-1, whose label warns of low blood sugar severe enough to cause seizures, raised pressure in the skull, tonsil and adenoid swelling, and cases of cancer in treated children. WADA bans IGF-1 and its analogues, including IGF-1 DES, at all times, and anti-doping labs test for it.
What it binds to, and what happens inside the body after that, step by step.
IGF-1 DES activates the same type 1 IGF receptor as native IGF-1. Its extra potency comes from barely binding IGF binding proteins, the absence of glutamic acid at position 3 being the key change, so more of it is free to reach tissues. In rats it stayed largely unbound in the blood, spread into a larger volume, reached the gut, skin and brain more than IGF-1, and was cleared about 4 times faster.
Human results and animal results are kept apart below. A result in rats tells you a mechanism is plausible. It does not tell you what happens in a person.
There are no published human studies of IGF-1 DES: no trials, no pharmacokinetics and no safety data. Rat studies show it is more potent than IGF-1 at restoring growth and preserving muscle protein, with the strongest effects on the gut, but it also clears from blood faster. A 1996 review by the group that studied it most said clinical uses had not yet been evaluated, and none have been since.
No human studies are among the key studies for IGF-1 DES. Everything known comes from animals or cells.
Diabetic rats, 7-day infusion of IGF-I, des(1-3)IGF-I or LR3-IGF-I
Both variants were 2.5 to 3 times more potent than IGF-I in restoring growth and raised muscle protein synthesis by up to 50%; none reduced sugar loss in urine.
Read the studyRats given radiolabeled tracers IV
Des(1-3)IGF-I stayed mostly unbound and cleared at 4.59 mL/min/kg vs 1.20 for IGF-I, with more reaching gut, skin and brain.
Read the studyRats after removal of 80% of the small intestine, 7-day infusion
At 0.96 mg/kg/day, des(1-3)IGF-I matched high-dose IGF-I for weight gain (20.8 vs 14.0 g with vehicle over 3 days) and nitrogen balance.
Read the studyRats with partial kidney removal, 7-day infusion
Improved weight gain and nitrogen balance, with des(1-3)IGF-I particularly effective at reducing muscle protein breakdown.
Read the studySpiked human serum; rats given a single 100 mcg/kg intramuscular dose; black-market products
Unchanged Des(1-3)-IGF-I was detectable in rats for 24 hours; black-market products showed oxidized, lower-quality peptide.
Read the studyTransgenic mice overproducing des(1-3)IGF-I in the mammary gland
By 23 months, 53% developed mammary adenocarcinomas, a 2- to 3-fold higher tumor rate than normal mice.
Read the studyWhen a new IGF-1 DES study in people is published, the daily email covers it.
These are questions the published research has not answered.
No product containing IGF-1 DES is approved as a medicine by the FDA.
Never developed as a human drug and never approved anywhere. The related molecule mecasermin (native IGF-1, Increlex) is FDA-approved for severe primary IGF-1 deficiency in children; IGF-1 DES is a different molecule. WADA S2.3 prohibits 'Insulin-like growth factor 1 (IGF-1, mecasermin) and its analogues' at all times, and doping labs have validated mass spectrometry tests that detect Des(1-3)-IGF-I in blood. A French anti-doping lab found signs of degraded, oxidized peptide in black-market IGF-1 analog products.
When the FDA or WADA changes IGF-1 DES's status, it's in the next morning's email.
No human half-life has been published for IGF-1 DES, so we do not draw a clearance curve. Half-lives quoted online for it are usually estimates from animal data.
No human study or approved label has published a dose for IGF-1 DES, so there is no table to show.
No dose of IGF-1 DES has been tested in a published human study or approved on a label. Numbers that circulate online come from animal studies scaled up by guesswork or from sellers. We do not reproduce them.
Which symptoms are expected and which mean stop and get help: side effects and red flags.
Tap a claim to see what the studies found.
The roughly 10-fold figure comes from cultured cells. In rats it was 2.5 to 3 times more potent at restoring growth, and no human data exist.
No human study has looked. In rats it spread into a larger volume than IGF-1 and reached gut, skin and brain, with its strongest effects on the gut.
Small amounts occur naturally, but injected doses have never been tested for safety in people. Native IGF-1 carries label warnings for hypoglycemic seizures and malignancy.
Rat studies show better nitrogen balance and less muscle protein breakdown, mostly in sick or surgically injured rats. No human study exists, and a year of native IGF-1 in older women did not add lean mass.
Sold freeze-dried as a research reagent. No published stability data for injection use.
No published stability data for any solution intended for injection.
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