Description
IGF-1 DES (also known as Des(1-3)IGF-1) is a synthetic, 67-amino acid analogue of the endogenous 70-amino acid human IGF-1 peptide. Native IGF-1 serves as a primary mediator of the somatotropic axis; however, its biological activity is heavily regulated and suppressed in physiological settings by a family of carrier proteins known as IGFBPs.
To overcome this regulatory mechanism in experimental models, IGF-1 DES is structurally truncated to remove the first three amino acids (glycine, proline, and glutamic acid) at the N-terminus. This specific modification drastically reduces the peptide’s binding affinity for secreted IGFBPs. Consequently, IGF-1 DES exhibits vastly increased unbound bioavailability and accelerated receptor binding kinetics compared to native IGF-1. It is widely utilized in laboratory settings to investigate acute, localized tissue regeneration, satellite cell activation, and hypertrophic cellular adaptations.
Biochemical Characteristics
Chemically, IGF-1 DES functions as an unbound agonist engineered for immediate, uninhibited receptor interaction.
- Sequence/Structure: 67-amino acid truncated synthetic polypeptide (lacking the N-terminal Gly-Pro-Glu sequence).
- Receptor Affinity: Binds specifically and with high affinity to the extracellular α-subunits of the IGF-1 Receptor (IGF-1R).
- Binding Protein Evasion: Demonstrates remarkably reduced affinity for IGFBPs compared to native IGF-1, preventing rapid neutralization in cell culture assays containing endogenously produced carrier proteins.
- Stability & Pharmacokinetics: Supplied as a lyophilized salt. While its evasion of IGFBPs vastly increases localized potency, its lack of protein binding results in a significantly shorter circulatory half-life than native or extended analogues, making it ideal for studying acute, rapid-onset signaling pathways.
Chemical Properties
| Property |
Specification |
| Molecule Name |
IGF-1 DES |
| Synonyms |
Des(1-3)IGF-1; Truncated IGF-1 |
| Molecular Weight |
~7365.5 g/mol |
| Form |
Lyophilized Powder |
| Purity |
≥99% (Verified via HPLC) |
| Solubility |
Soluble in water and organic solvents (refer to SDS) |
| Documentation |
COA available per lot; SDS available |
(Note: Exact Molecular Weights and Formulas should be verified per lot COA/SDS).
IGF-1 DES is strictly for laboratory research and is commonly employed in the following investigational areas:
Myoblast Proliferation & Acute Hypertrophy Models
IGF-1 DES is utilized as a highly potent mitogen in skeletal muscle models. Because it remains unbound by IGFBPs that are heavily secreted by damaged or inflamed tissues, researchers employ it to study the rapid activation and proliferation of satellite cells (myoblasts) following mechanically induced microlesions.
Cellular Bioavailability Assays
In vitro studies utilize IGF-1 DES to map the inhibitory role of endogenous IGFBPs. By comparing the cellular growth response of native IGF-1 against the unbound DES analogue in various cell lines (such as gastric cancer cells), researchers can quantify the specific regulatory impact of carrier proteins on tissue expansion.
Neuroprotection and Neuromodulation
Research investigating central nervous system (CNS) dynamics employs IGF-1 DES to study transport kinetics and neuroprotective pathways across the blood-brain barrier (BBB). Assays assess its ability to stimulate synaptic maturation markers independent of peripheral binding proteins.
Pathway / Mechanistic Context
The primary mechanism of action for IGF-1 DES in research settings revolves around the acute, uninhibited activation of the IGF-1 receptor.
- Receptor Activation: IGF-1 DES acts as an unbound agonist at the IGF-1R, inducing a conformational change that triggers autophosphorylation of the intracellular tyrosine kinase domains.
- Signal Transduction: This binding event rapidly activates the Phosphoinositide 3-kinase (PI3K)/AKT and the Ras-Mitogen-Activated Protein Kinase (MAPK/ERK) cascades.
- Resulting Flux: Due to the absence of IGFBP buffering, IGF-1 DES induces a rapid, concentrated spike in PI3K/AKT and MAPK/ERK signaling. This cascade acutely inhibits apoptotic pathways and drives a swift, potent mitogenic response, forcing accelerated cellular division and protein synthesis before the peptide is metabolically degraded.
Preclinical Research Summary
Published preclinical literature documents investigations of IGF-1 DES across multiple experimental models:
- Bioavailability and Potency: In vitro cellular proliferation assays consistently demonstrate that IGF-1 DES is significantly more potent at stimulating cell growth than equivalent concentrations of native IGF-1, entirely due to its ability to evade sequestration by cell-secreted IGFBPs.
- Pharmacokinetics: In vivo neurobiological models show that while IGF-1 DES possesses similar biological activity to native IGF-1 at the receptor level, its lack of protein binding results in a much shorter circulatory half-life and altered transport kinetics across the blood-brain barrier.
- Synaptic Maturation: Data from CNS assays indicate that the truncated peptide functions as an active metabolite with distinct neuroprotective effects, positively regulating excitatory synaptic markers such as synapsin 1 and post-synaptic density 95 (PSD-95).
Form & Analytical Testing
This material is produced via robust chemical synthesis and supplied as a lyophilized (freeze-dried) powder.
- Lyophilization: Removes water content under vacuum to maintain compound integrity and extend shelf-life.
- Identity Verification: Each lot undergoes Mass Spectrometry (MS) to confirm molecular weight and identity.
- Purity Verification: High-Performance Liquid Chromatography (HPLC) is performed to ensure the product meets the ≥99% purity standard required for reproducible research data.
Referenced Citations
References are provided for informational purposes only and are not clinical claims.
- Pan, W., Kastin, A. J., et al. (2000). Interactions of IGF-1 with the blood-brain barrier in vivo and in situ. Neuroendocrinology, 72(3), 171-178. https://doi.org/10.1159/000054584
- Vashi, N., et al. (2016). Insulin-Like Growth Factor 1 and Related Compounds in the Treatment of Childhood-Onset Neurodevelopmental Disorders. Frontiers in Neuroscience, 10, 450. https://doi.org/10.3389/fnins.2016.00450
- Guo, Y. S., et al. (1995). Insulinlike growth factor-binding protein modulates the growth response to insulinlike growth factor 1 by human gastric cancer cells. Gastroenterology, 108(4), 993-1004.https://pubmed.ncbi.nlm.nih.gov/7684715/
- Guenther, A., et al. (2008). Quantification of human insulin-like growth factor-1 and qualitative detection of its analogues in plasma using liquid chromatography/electrospray ionisation tandem mass spectrometry. Rapid Communications in Mass Spectrometry, 22(6), 871-881. https://doi.org/10.1002/rcm.3444
RESEARCH USE ONLY
This product is intended strictly for laboratory research use only. It is not for human or veterinary use. It is not intended for diagnosis, treatment, cure, or prevention of any disease. All purchases are subject to our Terms of Service and Purity Guarantee.
No COAs available for this product.
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