IGF-1 DES

preclinical

Also known as: DES(1-3) IGF-1, Des-IGF-1

IGF-1 DES (DES(1-3) IGF-1) is a naturally occurring truncated variant of insulin-like growth factor 1, lacking the N-terminal tripeptide Gly-Pro-Glu. This deletion reduces its affinity for IGF-binding proteins (IGFBPs), resulting in a significantly shorter half-life but enhanced local bioavailability and potency at the IGF-1 receptor. Its mechanism of action involves direct, high-affinity receptor activation in target tissues, promoting satellite cell proliferation, myogenesis, and protein synthesis with minimal systemic spillover. This localized action distinguishes it from full-length IGF-1, making it a candidate for site-specific anabolic effects. Preclinical research, primarily in rodent models, demonstrates that IGF-1 DES induces robust muscle hypertrophy and accelerates regeneration following injury, with effects confined to the site of administration. Studies show it upregulates markers of muscle repair (e.g., MyoD, myogenin) and increases muscle fiber cross-sectional area without significant systemic IGF-1 elevation or associated side effects. However, its short half-life and rapid clearance limit its utility for systemic applications, and no human clinical trials have been conducted to date. Clinically, IGF-1 DES remains an investigational compound with no approved therapeutic indications. Its potential applications are speculative and include localized muscle wasting conditions, post-surgical recovery, or cosmetic muscle enhancement, but safety and efficacy in humans are unestablished. The absence of pharmacokinetic and toxicity data in humans precludes any clinical recommendation. For research purposes only — not medical advice.

Key data

Category
Muscle & Performance
Administration
subcutaneous
Research status
preclinical
References
29
Tags
igf, anabolic, local

Research & studies

Transcriptomic Profile of Primary Culture of Skeletal Muscle Cells Isolated from Semitendinosus Muscle of Beef and Dairy Bulls
International journal of molecular sciences · 2020 · PubMed

825 upregulated and 1300 downregulated transcripts were common in both beef breeds compared to dairy breed.; The largest group of differentially expressed genes was involved in muscle organ development.; Beef breeds had higher expression of myogenesis genes (e.g., erbb-3, myf5, myog, des, igf-1, tgfb2) and contractile apparatus genes (e.g., acta1, myh3, myl1, tnnt2).; The expression profile of proliferating satellite cells is shared among beef breeds but distinct from dairy breeds.

Vitamin D and benign prostatic hyperplasia -- a review
The Canadian journal of urology · 2013 · PubMed

Vitamin D inhibits the RhoA/ROCK pathway and reduces cyclooxygenase-2 expression and prostaglandin E2 production in BPH stromal cells.; Higher dietary and supplemental vitamin D intake is associated with lower BPH prevalence.; Vitamin D analogues up to 6000 IU/day decreased prostate volume in BPH patients.; Pre-clinical trials showed vitamin D reduces BPH cell proliferation, even when induced by growth promoters like testosterone and IL-8.

Necdin-E2F4 interaction provides insulin-sensitizing effect after weight loss induced by gastric bypass surgery
Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery · 2013 · PubMed

Free IGF-1 levels were significantly greater in post-RYGB patients (2.55 ± 1.54 µg/L) than in pre-RYGB obese patients (1.32 ± 0.65 µg/L, P = .03) and similar to normal-weight controls (2.54 ± 1.27 µg/L).; Necdin and E2F4 gene expression in adipose tissue was significantly downregulated after RYGB compared with obese patients and similar to control levels.; In mature human adipocytes cultured in vitro, des-IGF-1 treatment induced dose-dependent downregulation of necdin and E2F4 gene expression (P = .01).; The insulin/IGF-1 signaling pathway is activated after RYGB and may account for decreased necdin expression, potentially representing a mechanism for resolution of insulin resistance after RYGB.

Enforced epithelial expression of IGF-1 causes hyperplastic prostate growth while negative selection is requisite for spontaneous metastogenesis
Oncogene · 2008 · PubMed

IGF-1(des) expression caused hyperplastic prostate growth in all transgenic mice.; Well-differentiated hyperplastic lesions did not progress to adenocarcinoma within one year.; Crossing PB-Des mice with a prostate cancer model delayed organ-confined tumor progression and metastasis in young mice.; IGF-1(des) was absent in poorly differentiated primary tumors and metastases, indicating negative selection against IGF-1 action.

Functional characterization of des-IGF-1 action at excitatory synapses in the CA1 region of rat hippocampus
Journal of neurophysiology · 2005 · PubMed

Des-IGF-1 (40 ng/ml) increased fEPSP slope by 40% in CA1 region.; Enhancement was postsynaptic and mediated by AMPA, not NMDA, receptors.; Effect was blocked by genistein and significantly reduced by PI3K inhibitors wortmannin and LY294002.; Acute des-IGF-1 action may contribute to cognitive improvement via AMPA receptor modulation.

Myogenin protein stability is decreased by BMP-2 through a mechanism implicating Id1
The Journal of biological chemistry · 2004 · PubMed

BMP-2 decreases myogenin protein stability, reducing its half-life to 50% independently of mRNA levels; Proteasome inhibitors abolish BMP-2-induced myogenin degradation; Forced Id1 expression causes myogenin degradation even in the absence of BMP-2; E47 overexpression blocks BMP-2's inhibitory effect and stabilizes myogenin through helix-loop-helix heterodimerization

Insulin-like growth factor-1 downregulates nuclear factor kappa B activation and upregulates interleukin-8 gene expression induced by tumor necrosis factor alpha
Biochemical and biophysical research communications · 2003 · PubMed

des-IGF-1 upregulated TNF alpha-induced IL-8 expression at protein, mRNA, and hnRNA levels; Upregulation involved RNA transcription, not RNA stabilization; des-IGF-1 partly inhibited TNF alpha-induced NF-kappa B activation and I kappa B alpha degradation through a PI-3K-dependent pathway; A C/EBP site cooperating with a NF-kappa B site on the IL-8 enhancer contributed to upregulation, with loss of C/EBP alpha binding in IGF-1-treated cells

Des(1-3)IGF-1 treatment normalizes type 1 IGF receptor and phospho-Akt (Thr 308) immunoreactivity in predegenerative retina of diabetic rats
International journal of experimental diabesity research · 2003 · PubMed

Type 1 IGF receptor immunoreactivity increased ~3-fold in INL and GCL of diabetic rats vs controls.; Phospho-Akt (Thr 308) immunoreactivity increased 5-fold in GCL and 8-fold in INL of diabetic rats.; Des(1-3)IGF-1 treatment significantly reduced immunoreactive cells in both layers.; Preliminary results suggested VEGF levels may also be reduced by the treatment.

Frequently asked questions

What is IGF-1 DES?

IGF-1 DES (DES(1-3) IGF-1) is a naturally occurring truncated variant of insulin-like growth factor 1, lacking the N-terminal tripeptide Gly-Pro-Glu. This deletion reduces its affinity for IGF-binding proteins (IGFBPs), resulting in a significantly shorter half-life but enhanced local bioavailability and potency at the

How does IGF-1 DES work?

Truncated IGF-1 variant with high local potency and short half-life, studied for site-specific muscle growth.

What is the research status of IGF-1 DES?

IGF-1 DES is currently classified as preclinical, with 29 research references on record. This is for research purposes only and is not medical advice.

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