IGF-1 DES 1mg

What is IGF-1 DES?

IGF-1 DES is a truncated version of IGF-1 in which the tripeptide Gly-Pro-Glu is absent from the N-terminus end of the protein. It is actually a naturally occurring variant of IGF-1 and has been found in the human brain, cow colostrum, and pig uterine tissue. IGF-1 DES is 10 times more potent than IGF-1 in stimulating hypertrophy and proliferation of cells because it is not affected by IGF-1 binding proteins and therefore is more bioavailable. There is interest in using the peptide to induce anabolism in catabolic conditions (e.g., chronic illness) and in the treatment of inflammatory bowel disease.

IGF-1 DES has also been of keen interest in the treatment of a number of neurological and neurodevelopmental conditions. Researchers investigating autism and autism spectrum disorders have found that IGF-1 and its analogues have potent effects on the synaptic health of neurons. In animal models of autism, IGF-1 DES and IGF-1 have relieved symptoms and improved a number of the behavioral aspects of the condition.

IGF-1 DES Research

IGF-1 DES Is More Potent Than IGF-1

IGF-1 DES is missing just three amino acids from its N-terminal end, yet this subtle modification significantly enhances its biological properties. Research indicates that IGF-1 DES does not bind effectively to IGF-1 binding proteins (IGFBPs) found in the blood and various tissues throughout the body. This results in greater availability of the peptide for binding to critical receptors, making IGF-1 DES more potent—achieving the same effects at lower doses compared to IGF-1 itself.

Studies conducted on pigs and marmosets suggest that IGF-1 DES is 2-3 times more effective than IGF-1 in lowering blood sugar levels. This increased potency also extends to its anabolic effects on skeletal muscle and its neuroprotective properties.

One advantage of binding to IGFBPs is the extension of peptide activity due to reduced clearance from circulation. However, IGF-1 DES exhibits a unique efficacy profile: it has a faster onset of action, higher peak activity, and quicker withdrawal compared to IGF-1. This makes it particularly promising for research into hyperglycemic conditions and other metabolic studies.

IGF-1 DES Research and Neurological Disease

It is well-established that IGF-1 plays a crucial role in neuron growth, differentiation, and survival. As a major factor in synaptic formation, IGF-1 significantly influences learning, memory, and overall cognitive function. It is especially critical for the development and maintenance of mature synapses, ensuring effective communication between neurons.

Research indicates that IGF-1 is essential for achieving proper levels of presynaptic synapsin-1, a protein that regulates neurotransmitter release. This regulation is vital for efficient synaptic signaling and brain communication. Additionally, IGF-1 supports the post-synaptic PSD-95 protein, which maintains synaptic structure and stability.

Without adequate IGF-1 activity, synaptic development is disrupted, leading to deficits in motor skills, behavior, cognitive functioning, and language development. These findings underscore the importance of IGF-1 DES in research focused on neurodevelopmental disorders, cognitive impairments, and neurological health.

IGF-1 and its analogues, including IGF-1 DES, have been extensively studied for their potential benefits in various neurological conditions, including Rett Syndrome and Chromosome 22 Deletion Syndrome. Research indicates that these peptides contribute to protecting excitatory synapses in the brain and preserving neuron density, which are critical for maintaining healthy brain function.

One of the significant findings is that IGF-1 reduces the toxic effects of NMDA over-stimulation, which can lead to excitotoxicity—a process that causes neuron death. By safeguarding neurons against this damage, IGF-1 DES has shown promise in animal studies, leading to its consideration as an experimental treatment for neurological disorders.

Clinical trials of IGF-1 in Multiple Sclerosis (MS), Amyotrophic Lateral Sclerosis (ALS), Parkinson’s Disease (PD), and Alzheimer’s Disease (AD) have yielded varied results:

• In ALS, IGF-1 treatment demonstrated significant reductions in disease progression, increased muscle strength, improved respiratory function, and enhanced quality of life.
• In Multiple Sclerosis (MS), clinical trials showed minimal impact, indicating a different therapeutic pathway may be required.
• For Parkinson’s Disease (PD), while human trials are pending, animal studies have indicated that IGF-1 can protect dopaminergic neurons and improve behavioral outcomes.
• Research in Alzheimer’s Disease (AD) is ongoing, with IGF-1 DES being explored for its neuroprotective capabilities and potential to slow cognitive decline.

IGF-1 DES May Have Cognitive Benefits in Age

While IGF-1 is crucial during childhood development, its role remains significant in adults as well. In adult brains, IGF-1 is naturally modified into shorter forms, highlighting the potential of analogues like IGF-1 DES for therapeutic applications. These modified forms, including IGF-1 DES, demonstrate enhanced penetration of the blood-brain barrier, making them more effective when administered exogenously.

Studies have shown that IGF-1 and its analogues contribute to reducing neuronal death and protecting neurons from damage caused by stroke, Alzheimer’s disease, Parkinson’s disease, and other neurodegenerative conditions. This neuroprotective effect underscores the potential of IGF-1 DES as a promising candidate for addressing adult neurological disorders.