The record
| Class | growth factor |
|---|---|
| Also known as | Des(1-3)IGF-1, Des-IGF-1, Truncated IGF-1 |
| Chain length | - |
| Molecular weight | 7,371.5 Da |
| Half-life | 20-30 minutes |
| Route | Intramuscular (site-specific) |
| Studied for | - |
| Research use | Muscle hypertrophy studies; Local muscle growth (site-specific); Muscle cell culture |
| What has been shown | 10-fold more potent than IGF-1 in vitro; Enhanced local muscle growth; Minimal systemic effects due to short half-life; Satellite cell activation |
| How it works | N-terminally truncated form of IGF-1 (missing GPE tripeptide). Enhanced IGF-1R binding due to minimal IGFBP sequestration. Activates PI3K/Akt and Ras/MAPK/ERK pathways. ~10-fold more potent than native IGF-1 in vitro. Preferential binding to lactic acid-damaged muscle cells. Promotes satellite cell activation and muscle hyperplasia. |
| Patent status | Various research patents |
| Regulatory status | Research use only - NOT approved |
Blank = not established in the record. Nothing is estimated to fill a gap.
Where it is matched
- Muscle Hypertrophy / Anabolic Signaling (affection, 64%)
- GH Pulsatility Environment (affection, 32%)
- Adult GH deficiency (illness, 30%)
- Anti-aging therapy (illness, 30%)
- Cardiac repair after myocardial infarction (illness, 40%)
- Duchenne muscular dystrophy (illness, 60%)
- Muscle wasting conditions (illness, 48%)
- Neuromuscular diseases (illness, 60%)
- Pediatric growth hormone deficiency (illness, 30%)
- Post-injury muscle recovery (illness, 40%)
- Post-stroke recovery (illness, 40%)
- Soft tissue repair (illness, 40%)
- Muscle loss or weakness (symptom, 67%)