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IGF-1 DES research

What published studies found for IGF-1 DES: 10 papers, 0 in humans, with sample sizes and key results.

C
Mostly animal studies
Why: Never tested in humans; rat, mouse and pig studies show anabolic effects, with negative neuroprotection results and tumour signals in transgenic mice.

IGF-1 DES (des(1-3)IGF-I) is a naturally occurring truncated IGF-I that is more potent than IGF-I in cell and rodent studies; all in-vivo evidence is from rats, mice and pigs, mostly from the early 1990s. It has never been evaluated in human trials, and animal and cell studies raise growth-promoting (tumour) concerns.

✓ 4 positive✗ 4 negative? 2 inconclusive

No human safety data in the published literature; animal and cell studies show potent mitogenic effects, including promotion of mammary tumours in transgenic mice.

US compounding: Not compoundable. Not an FDA-approved drug and not nominated for FDA's 503A bulks list, so US pharmacies can't legally compound it. Status for every peptide.

Browse and filter these papersIGF-1 DES prices and vendors

Reviews

? InconclusivereviewInt J Biochem Cell Biol · 1996

Des(1-3)IGF-I: a truncated form of insulin-like growth factor-I.

No new dataNarrative review

Review noting des(1-3)IGF-I is ~10-fold more potent than IGF-I in cultured cells due to weak IGF-binding-protein binding, with anabolic effects mainly in gut tissue in vivo; clinical use had not been evaluated.

Studied
Literature on des(1-3)IGF-I, a truncated IGF-I variant
Main outcome
Potency, biology and potential clinical use
Authors' conclusion
Des(1-3)IGF-I is generally about 10-fold more potent than IGF-I in cultured cells due to reduced IGFBP binding, with selective anabolic effects in gut in vivo. Clinical opportunities have not yet been evaluated.
Limitations
No clinical data.
PubMed 8930132DOI

Animal & lab studies

✓ PositiveanimalBiochem J · 1991

Increased weight gain, nitrogen retention and muscle protein synthesis following treatment of diabetic rats with insulin-like growth factor (IGF)-I and des(1-3)IGF-I.

AnimalsAnimal infusion study of hGH, IGF-I, des(1-3)IGF-I and insulin7 days

In diabetic rats, 7 days of des(1-3)IGF-I improved weight gain and nitrogen retention (~70% of insulin's effect) via increased muscle protein synthesis, without fixing glucose control.

Key resultIGF-I gave about 30% of the improvement achieved with insulin (significant in only one of two experiments, P < 0.05); a 2.5-fold higher IGF-I dose or des(1-3)IGF-I gave approx. 70% of insulin's effect.
Studied
Streptozotocin-induced diabetic rats
Compared with
Vehicle controls; insulin; hGH
Main outcome
Body weight, nitrogen retention, muscle protein synthesis
Authors' conclusion
IGF peptides stimulate muscle protein synthesis and improve nitrogen balance in diabetic rats without improving glucosuria; des(1-3)IGF-I is at least as potent as IGF-I.
Limitations
Rat model; group sizes not stated in abstract.
PubMed 1710892DOIFree full text
✓ PositiveanimalMiner Electrolyte Metab · 1992

Insulin-like growth factor I and its variant, des(1-3)IGF-I, improve nitrogen balance and food utilization in rats with renal failure.

5/6 nephrectomy rats, 8 per group (4 groups); 7 sham controlsAnimal study of subcutaneous IGF-I (0.9 or 2.2 mg/kg/day) or des(1-3)IGF-I (0.9 mg/kg/day) by osmotic pump7 days

In rats with partial kidney removal, des(1-3)IGF-I improved food utilization 13-16%, cut nitrogen excretion 24% and lowered serum urea 25%, without altering carcass composition.

Key resultFood utilization improved 13-16% in all peptide groups; nitrogen excretion fell 24% with des(1-3)IGF-I and 16% and 18% with low- and high-dose IGF-I.
Studied
Rats after 5/6 nephrectomy (renal failure model)
Compared with
Vehicle-treated nephrectomized rats; sham-operated controls
Main outcome
Nitrogen balance, food utilization, serum urea, muscle protein degradation
Authors' conclusion
IGF-I, and more particularly des(1-3)IGF-I, may be efficacious in overcoming impaired growth in renal failure.
Limitations
Rat model; 7-day study.
PubMed 1465072
✓ PositiveanimalAm J Physiol · 1991

IGF-I and the truncated analogue des-(1-3)IGF-I enhance growth in rats after gut resection.

AnimalsAnimal study of IGF-I (0.96 or 2.4 mg/kg/day) or des-(1-3)IGF-I (0.96 mg/kg/day) by osmotic pump7 days

In rats after removal of 80% of the small bowel, des(1-3)IGF-I improved weight gain and nitrogen balance; kidney and thymus weights also increased.

Key resultNitrogen balance over the last 3 days was 242 ± 14 mg/d (high-dose IGF-I) and 217 ± 13 mg/d (des-(1-3)IGF-I) vs 153 ± 21 mg/d in controls (P less than 0.05).
Studied
170 g rats after resection of 80% of jejunum plus ileum
Compared with
Vehicle and low-dose IGF-I
Main outcome
Weight gain and nitrogen balance
Authors' conclusion
High-dose IGF-I and des-(1-3)IGF-I enhanced weight gain and nitrogen balance after gut resection in rats; effects partly explained by reduced muscle protein breakdown.
Limitations
Rat model; abstract truncated.
PubMed 1996625DOI
✓ PositiveanimalJ Endocrinol · 1990

Enhanced potency of truncated insulin-like growth factor-I (des(1-3)IGF-I) relative to IGF-I in lit/lit mice.

AnimalsAnimal study comparing daily injections of IGF-I and des(1-3)IGF-I3 weeks

In GH-deficient mice, 3 weeks of des(1-3)IGF-I increased body length at a tenth of the effective IGF-I dose, with increased kidney and heart weights; body weight did not change significantly.

Key result30 µg IGF-I, 30 µg des(1-3)IGF-I or 3 µg des(1-3)IGF-I daily increased length substantially more than in controls or 3 µg IGF-I; body weight changes were not statistically significant.
Studied
lit/lit (GH-deficient) mice
Compared with
Controls; IGF-I
Main outcome
Total length, nose-rump length, body and organ weights
Authors' conclusion
The higher potency of des(1-3)IGF-I seen in cultured cells also applies in vivo in at least one GH-deficient mouse strain.
Limitations
One mouse strain; group sizes not stated in abstract.
PubMed 2280209DOI
✗ NegativeanimalOncogene · 2000

Cooperative interaction between mutant p53 and des(1-3)IGF-I accelerates mammary tumorigenesis.

AnimalsTransgenic mouse mammary tumorigenesis studyUp to 23 months of age

Transgenic mice overexpressing des(1-3)IGF-I in the mammary gland developed pre-cancerous lesions, and 53% developed mammary adenocarcinomas by 23 months; mutant p53 accelerated tumour onset.

Key resultBy 23 months, 53% of WAP-DES mice developed mammary adenocarcinomas; tumor latency was reduced by 8 months in bitransgenic mice.
Studied
Transgenic mice overexpressing des(1-3)hIGF-I (WAP-DES) and/or mutant p53 (p53172R-H)
Compared with
Nontransgenic and p53172R-H mice
Main outcome
Mammary tumor incidence and latency
Authors' conclusion
Overexpression of des(1-3)hIGF-I increases mammary intraepithelial neoplasia and stochastic tumors, and mutant p53 accelerates tumors with genomic instability. This is transgenic overexpression, not drug dosing.
Limitations
Transgenic overexpression model; not peptide administration.
PubMed 10702797DOI
✗ NegativeanimalEndocrinology · 1996

The effects of insulin-like growth factor (IGF)-1, IGF-2, and des-IGF-1 on neuronal loss after hypoxic-ischemic brain injury in adult rats: evidence for a role for IGF binding proteins.

Groups of 10 to 20 rats per treatmentAnimal experiment, intraventricular dosingNeuronal loss assessed 5 days later

In adult rats after hypoxic-ischemic brain injury, central IGF-1 reduced neuronal loss, but des-IGF-1 at 2 or 20 micrograms did not (only a non-significant trend at 150 micrograms), pointing to a role for IGF binding proteins.

Key resultIGF-1 (20 micrograms) reduced neuronal loss in all regions (P < 0.01); des-IGF-1 at 2 and 20 micrograms did not.
Studied
Adult rats with unilateral hypoxic-ischemic brain injury
Compared with
IGF-1, IGF-2, vehicle
Main outcome
Neuronal loss in cortex, striatum, hippocampus and other regions
Authors' conclusion
Binding proteins may target IGF-1's neuroprotective action; IGF-2 may antagonise IGF-1 by displacing it from them.
Limitations
Rat study of des-IGF-1 as a comparator; 1996.
PubMed 8603600DOI
✗ NegativeanimalBrain Behav · 2026

Prenatal (1-3)IGF-1 Treatment Is Ineffective and Behaviorally Detrimental in a Rat Model of Cortical Malformation.

AnimalsAnimal study with in utero MRI and behavioural testingPrenatal plus prolonged early postnatal treatment

In a rat model of cortical malformation, prenatal and early postnatal (1-3)IGF-1 did not improve brain growth, neurometabolites or seizure susceptibility, and long-term exposure impaired spatial working memory.

Studied
Rat offspring in a MAM-induced cortical malformation model
Compared with
Untreated / vehicle groups
Main outcome
Brain morphology, neurometabolites, seizure susceptibility, behaviour
Authors' conclusion
No benefit in any paradigm and detrimental behavioural effects, cautioning against assuming earlier or longer IGF-1-based treatment is beneficial.
Limitations
Animal model of one specific malformation.
PubMed 41992821DOIFree full text
FIGURE 5: Effects of long‐term (1–3)IGF‐1 treatment on behavior in MAM‐exposed rats. (A) Y‐maze testing at P40 revealed a significant reduction in nov
FIGURE 5. From PMC13087530, CC BY (terms); resized.
✗ NegativeanimalProc Natl Acad Sci U S A · 1995

Cardioprotective effect of insulin-like growth factor I in myocardial ischemia followed by reperfusion.

AnimalsAnimal experiment20 min ischemia plus 24 h reperfusion

In rats with myocardial ischemia-reperfusion, IGF-I reduced heart injury and cardiomyocyte apoptosis, but this protection was not seen with des-(1-3)-IGF-I.

Studied
Rats with myocardial ischemia followed by reperfusion
Compared with
IGF-I; vehicle
Main outcome
Creatine kinase loss, neutrophil accumulation, myocyte apoptosis
Authors' conclusion
IGF-I protected ischemic myocardium; the abstract states the protective effect was not observed with des-(1-3)-IGF-I.
Limitations
Des-(1-3)-IGF-I was only a comparator in a study of IGF-I; 1995.
PubMed 7644533DOIFree full text
? Inconclusivein vitroMol Cell Endocrinol · 2002

Des (1-3) IGF-I-stimulated growth of human stromal BPH cells is inhibited by a vitamin D3 analogue.

Cells / labIn vitro cell study of Des(1-3)IGF-I and a vitamin D3 analogue

In human benign prostatic hyperplasia stromal cells, des(1-3)IGF-I acted as a potent mitogen, stimulating growth and inhibiting apoptosis.

Studied
Human stromal benign prostatic hyperplasia (BPH) cells
Main outcome
BPH cell proliferation, apoptosis, bcl-2 expression
Authors' conclusion
Des(1-3)IGF-I is a potent mitogen for BPH stromal cells, stimulating growth and inhibiting apoptosis; a vitamin D3 analogue inhibited this and induced apoptosis, so such analogues might be considered for BPH treatment.
Limitations
In vitro only.
PubMed 12573816DOI

Verdicts are judged on each paper's own main outcome; grades run from A (strong human evidence) to D (little or none). Details are read from the abstracts, and figures are reproduced only from openly licensed full texts. Not medical advice.