IGF-DES

What is IGF-1 DES?

IGF-1 DES represents a modified form of Insulin-like Growth Factor-I (IGF-I) where the tripeptide Gly-Pro-Glu has been removed from the N-terminus portion of the molecule. This variant occurs naturally and can be found in human brain tissue, cow colostrum, and pig uterine tissue.

Compared to standard IGF-I, IGF-1 DES demonstrates 10 times greater potency in promoting hypertrophy and cellular proliferation. This enhanced potency stems from its inability to bind with IGF-I binding proteins (IGFBPs), resulting in superior bioavailability. The peptide shows promise for inducing anabolic effects in catabolic conditions (such as chronic illness) and for addressing inflammatory bowel diseases.

IGF-1 DES has attracted significant attention for treating various neurological and neurodevelopmental disorders. Scientists studying autism and autism spectrum disorders have discovered that IGF-1 and its related compounds can positively influence synaptic neuron health. Animal studies involving autism have shown that both IGF-1 DES and IGF-I successfully alleviated symptoms and enhanced multiple behavioral measures.

IGF-1 DES Structure

Chemical Details

• Formula: C317H497N91O101S7
• Molecular Weight: 7076.6 g/mol
• Purity (HPLC): Typically greater than 98%
• Sequence: F-V-N-Q-H-L-C-G-S-H-L-V-E-A-L-Y-L-V-C-G-E-R-G-F-Y-F-N-K-P-T-G-Y-G-S-S-S-R-R-A-P-Q-T-G-I-V-D-E-C-C-F-R-S-C-D-L-R-R-L-E-M-Y-C-A-P-L-K-P-A-K-S-A

IGF-1 DES Research

IGF-1 DES Demonstrates Greater Potency Than IGF-I

IGF-1 DES consists of only three amino acids removed from the N-terminal end, yet this minor modification creates substantial differences. Studies indicate that IGF-1 DES shows no binding affinity for IGF-I binding proteins (IGFBPs) present in blood and various tissues throughout the body. Consequently, at physiological pH levels, all circulating IGF-1 DES remains free and available to bind with its receptors. This gives IGF-1 DES significantly more powerful effects at lower concentrations compared to standard IGF-I. Research involving pigs and mammalian cell cultures has validated these enhanced potency characteristics [1].

The extended action of IGF-1 DES represents one of its key advantages, resulting from reduced clearance from circulation. IGF-1 DES exhibits considerably longer onset of action, higher peak activity levels, and more prolonged withdrawal compared to standard IGF-I [2], [4]. Such an efficacy profile offers potential benefits for treating hyperglycemic conditions.

Pig studies reveal that IGF-1 variants with reduced IGFBP affinity produce more pronounced growth effects. The anabolic properties of IGF-1 DES remain effective even in restricted calorie environments. Research involving rats demonstrates that administering just 14 days of IGF-1 is sufficient to generate significant improvements in body weight, nitrogen balance, and blood conversion efficiency [3]. Being a more potent and longer-lasting anti-hyperglycemic agent, IGF-1 DES reduces blood sugar levels more rapidly following administration. This forms part of the rationale for researcher interest in utilizing IGF-1 DES as a potential treatment for Type II diabetes.

IGF-1 DES Research and Neurological Disease

Scientific evidence has long established that IGF-I produces significant effects on neuron growth, differentiation, and survival. The peptide represents a crucial component in learning, memory development, and related functions. IGF-I holds particular importance for proper functioning and maintenance of mature neurons. Research demonstrates that IGF-I is essential for achieving appropriate levels of pre-synaptic vesicles, which are structures that regulate neurotransmitter release. Without adequate IGF-I, synaptic development becomes disrupted, which affects synaptic structure maintenance [6], [7].

IGF-1 DES and Autism

Studies indicate that IGF-I may serve as an important factor in numerous neurological disorders, including autism. Children with autism display reduced brain concentrations of IGF-I compared to neurotypical children. Mouse model research on autism suggests that IGF-II and its analogues like IGF-1 DES can reverse all behavioral deficits linked to the condition. Mice receiving IGF-II for only five days showed sustained improvements in compulsive conditioning, reduced repetitive/compulsive behaviors, enhanced grooming patterns, and improved spatial memory processing. These positive outcomes remained stable after treatment cessation [8], [9].

IGF-1 DES Research and Immune Function

Various immune cells, including B cells, T cells, dendritic cells, and neutrophils, possess IGF-I receptors on their surface. Research demonstrates that IGF-1 DES can enhance immune system function. IGF-1 DES shows greater potency in stimulating neutrophils and macrophages to eliminate pathogens. This enhanced effect could serve as an effective complement to antibiotic and alternative antimicrobial treatments in infection management [12].

IGF-1 DES May Have Cognitive Benefits in Age

IGF-I plays a crucial role in both adult and child development. Molecules similar to IGF-1 DES also cross the blood-brain barrier more efficiently than regular IGF-I. In adults, both IGF-1 and its variants have demonstrated ability to decrease beta-amyloid accumulation in the brain, potentially aiding conditions like Alzheimer's disease and Parkinson's disease, among others [10]. According to research findings, IGF-1 DES produces approximately a 40% enhancement in excitatory synaptic transmission [11].

IGF-1 DES Is a New Contender

IGF-1 DES shows promise for treating various conditions related to IGF-I, including enhanced skeletal muscle development and protection of neurons. The peptide differs in that it does not bind to IGFBPs, which allows it to cross the blood-brain barrier when administered subcutaneously. IGF-1 DES generates significantly higher levels of interest among researchers in studies examining neurodevelopment, stroke, cancer, wound healing treatment, autism, and diabetes management.

IGF-1 DES demonstrates moderate side effects. Oral and injectable forms show excellent subcutaneous bioavailability in mice. Dosage scaling from mice to humans does not translate directly to humans. IGF-1 DES offers benefits beyond standard IGF-I as a licensed pharmaceutical available only through licensed researchers.

IGF-1 DES Research and Cancer

Compelling cancer cells to differentiate could reduce growth rates by inducing differentiation. Research involving chicken leukemia cells demonstrates that cells treated with IGF-1 DES and IGF-I stop tumor growth by promoting differentiation [14].

IGF-1 DES May Improve Wound Healing

Skin dermal fibroblasts represent the primary cells responsible for tissue repair following injury. Scientific research has established that IGF-1 DES can positively impact healing processes. By administering peptides unaffected by IGF-I, it becomes possible to reduce inflammation and potentially enhance healing in compromised tissue or environments with reduced blood supply. In research contexts, this can accelerate wound healing processes [13].

Article Author

The above content was researched, edited, and organized by Dr. Logan, M.D. Dr. Logan maintains a doctorate degree from Case Western Reserve University School of Medicine and B.S. credentials in molecular biology.

Scientific Journal Author

Dr. Clemmons' clinical practice focuses on growth hormone and IGF-I research, particularly concerning patients with hypopituitarism and those with pituitary tumors displaying hyperfunction. His fundamental research examines understanding molecular and cellular pathways through which insulin-like growth factors promote cellular proliferation and differentiation. He conducts clinical investigations involving new methods for evaluating the effects of these factors in patients with diabetic nephropathy and retinopathy.

Dr. Clemmons maintains recognition as a prominent scientist in IGF-I and DES research and development. He does not participate in product endorsement, explanation, or advocacy for purchasing, selling, or utilizing this product for any purpose. No affiliation, relationship, implied or explicit, exists between Peptide Sciences and Dr. Clemmons. Dr. Clemmons is referenced here under the referenced citations for acknowledgment, recognition, and crediting the extensive research and development work.

Referenced Citations

Citation #

Summary of Topic

Year

[1]

Truncated variant of IGF-I (Des(1-3)IGF-I)

1996

[2]

IGF-I variants and hypoglycaemic action in pigs/monkeys

1997

[3]

In vivo actions of IGF analogues with reduced IGFBP affinities in pigs

1995

[4]

Effects of IGFBP interactions on IGF clearance and activities

1993

[5]

New experimental treatments for social domain in autism

2014

[6]

Therapeutic potential of IGF-1 in CNS disorders

2016

[7]

IGFs in the pathogenesis of neurological diseases in children

2017

[8]

IGF-II reverses autism-like phenotypes in mice via mTOR pathway

2018

[9]

Autism and the synapse: emerging mechanisms

2015

[10]

Neuroprotective effects of short peptides from IGF-1

2007

[11]

Functional characterization of des-IGF-1 action in rat hippocampus

2005

[12]

Effects of IGF analogues on bovine immune cell function

1993

[13]

Cytokines modulate fibroblast sensitivity to IGF-I by altering IGFBPs

1993

[14]

IGF-I and IGF-I on differentiation of human colon cancer cells

1992

[15]

General reference for research in the field

2004