IGF-1 DES (1mg)

$89.00

Size: 1mg
Contents: IGF-1 DES (1mg)
Form: Lyophilized powder
Purity: >99%
SKU: P-IGF1DES-1

FREE Shipping on $200+ orders

FREE Bacteriostatic Water (30ml) on $200+ orders

Discount per Quantity

QuantityDiscountPrice
5 - 85%$84.55
9 +10%$80.10
SKU: P-IGF1DES-1 Category: Tag:

 

IGF-1 DES Peptide

Insulin-like growth factor-1, IGF-1, is an endogenous hormone peptide considered to be involved in several anabolic bodily functions.(1) Several forms of IGF-1 occur naturally as well as some are developed artificially for their research potential, which appears to have the same or more potency as IGF-1 itself. IGF-1 DES is one such analog of IGF-1.  IGF-1 DES was developed to be identical structurally to IGF-1, truncated with the three amino acids absent from the N-terminus.(3)

Researchers posit that this absence of the tripeptide Gly-Pro-Glu may make IGF-1 DES 10x more potent than any stimulation IGF-1 may provide. Since the tripeptide is absent, researchers suggest that IGF-1 DES might not easily bind with the IGF-1 binding receptors, which may result in higher proliferation and differentiation of tissue cells.(3)

Overview

Studies(5) have suggested that IGF-1 DES functions through different routes as follows: it may possibly stimulates CA1 fEPSPs (Excitatory Postsynaptic Potential). The flow of the positively charged ions into the cell (thereby causing the excitatory post synaptic potential) quite possibly results in the opening of various ion channels. Experiments in presented IGF-1 DES for 15 minutes resulted in a 40% slope increase of CA1 fEPSPs, suggesting that the peptide may exert a function through acting on and stimulating ion channels.

Further experimental studies suggest that IGF-1 DES may stimulate excitatory synaptic transmission, mainly mediated through the PI3K pathway. To explore the potential excitatory transmission in the CA1 region, researchers conducted an experiment(5) where IGF-1 DES was introduced to brain cells, alongside either with tyrosine inhibitor or PI3K inhibitor compounds. Both tyrosine kinase and PI3K are considered by the scientific community to be enzymatic cells involved in cell growth, differentiation and proliferation. Researchers stated in the study that after presenting these three compounds, it was observed that tyrosine kinase inhibitors did not appear to interfere with IGF-1 DES functioning, however, PI3K inhibitor compounds were reported to drastically reduce the fEPSP slope.

 

Research and Clinical Studies

IGF-1 DES and Neurological Action

A study(7) was conducted on the SHANK3 depleted mice who were given IGF-1 and its analogs for two weeks. Daily peptide presentation for two weeks ultimately resulted in what researchers called the reversal of several ‘unwanted’ functions which are considered to be a direct result of a SHANK3 deficiency, including deficits in motor signaling and performance.

In another study,(7) a mouse model induced with Rett Syndrome was presented with IGF-1 and its analogs. IGF-1 analogs appeared to result in enhanced synaptic development and inhibition of phenotype defects. Researchers in both studies indicated that IGF-1 and its analogs may the potential to inhibit the development and progression of neurological deterioration.

IGF1 DES and Autistic Mice Models

Autism spectrum disorder(9) is a rare genetic condition associated with poor brain development. Research has suggested that this ailment is probably caused by deficits in the synaptic development and is pathologically similar to other ailments such as tuberous sclerosis.(10)

A study(11) was conducted on autistic mouse models that were given IGF-II and its analogs, such as IGF-1 DES. Within five days, researchers stated that the peptide appeared to result in enhanced social interaction and reduced compulsive behavior. The cognitive functioning of the mice also appeared to improve significantly.

IGF-1 DES and Cognition

Research(12) has suggested that IGF-1 peptide hormone may be influential growth and development. While most of the peptides originate from the liver, there are some additional short peptide isoforms that are suggested to be potent as neuroprotective agents, and their mechanism does not solely depend on the IGF-1 receptors. These short isoforms, such as IGF-1 DES, have been suggested to easily cross the blood brain barrier and may be highly stable.  A study(13) was conducted on the hippocampal brain cells of the young rats to identify the potential of the IGF-1 DES peptide on the excitatory synapses of the brain region. IGF-1 DES presentation reportedly resulted in a 40% increase in the excitatory synaptic responses primarily through AMPA receptors, possibly enhancing cognitive function. Further research is necessary to validate this hypothesis.

IGF-1 DES and Immune Function

This study(14) was conducted to determine the potential of IGF-1 isoforms, namely IGF-1 DES and long R3 IGF-1, on immune function by acting on the mononuclear and neutrophil cells. Cells were preincubated with a standard agent (no IGF-1), IGF-1 DES and Long R3 IGF-1. As a result of this, there appeared to be higher hydrogen peroxide release from these cells by 65%, 64% and 32% respectively.

IGF-1 DES and Carcinogenic Cells

Scientists consider that of the primary issues with carcinogenic cells is that they remain undifferentiated or exist at very early stages of cell differentiation, making them difficult to isolate and destroy. By differentiating these cancer cells, tumor development might be inhibited. Research(15) has suggested that when IGF-1 DES is presented in nanomolar amounts in carcinogenic HT29-D4 cells, it may force these cells to differentiate into a phenotype. Correspondingly, early presentation of IGF-1 DES might also impart moderate inhibition of cell proliferation of the HT29-D4 cells. The researchers in this study suggested that IGF-1 DES may have the potency to differentiate certain types of cancer cells (in this case, colon carcinoma HT29-D4 cells).

IGF-1 DES peptide is available for research and laboratory purposes only. Please review and adhere to our Terms and Conditions before ordering.

References:

  1. Anderson, Lindsey J et al. “Use of growth hormone, IGF-I, and insulin for anabolic purpose: Pharmacological basis, methods of detection, and adverse effects.” Molecular and cellular endocrinology vol. 464 (2018): 65-74. doi:10.1016/j.mce.2017.06.010. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5723243/
  2. IGF-1 (Insulin-like Growth Factor 1) Test. https://medlineplus.gov/lab-tests/igf-1-insulin-like-growth-factor-1-test/
  3. Ballard FJ, Wallace JC, Francis GL, Read LC, Tomas FM. Des(1-3)IGF-I: a truncated form of insulin-like growth factor-I. Int J Biochem Cell Biol. 1996 Oct;28(10):1085-7. https://pubmed.ncbi.nlm.nih.gov/8930132/
  4. Yakar, S et al., 40 YEARS OF IGF1: Insulin-like growth factors: actions on the skeleton (Jul 2018). Journal of Molecular Endocrinology, vol. 61 Issue 1. https://doi.org/10.1530/JME-17-0298
  5. Melinda M. Ramsey et al, Functional Characterization of Des-IGF-1 Action at Excitatory Synapses in the CA1 Region of Rat Hippocampus, 01 Jul 2005. https://journals.physiology.org/doi/full/10.1152/jn.00768.2004
  6. Phelan-McDermid Syndrome: Causes and Symptoms. https://www.massgeneral.org/children/phelan-mcdermid-syndrome
  7. Canitano, Roberto. “New experimental treatments for core social domain in autism spectrum disorders.” Frontiers in pediatrics vol. 2 61. 20 Jun. 2014. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4064155/
  8. Rett Syndrome. https://www.mayoclinic.org/diseases-conditions/rett-syndrome/symptoms-causes/syc-20377227
  9. Autism Spectrum Disorder. https://www.mayoclinic.org/diseases-conditions/autism-spectrum-disorder/symptoms-causes/syc-20352928
  10. Ebrahimi-Fakhari D, Sahin M. Autism and the synapse: emerging mechanisms and mechanism-based therapies. Curr Opin Neurol. 2015 Apr;28(2):91-102. https://pubmed.ncbi.nlm.nih.gov/25695134/
  11. Adam B. Steinmetz et al, Insulin-Like Growth Factor II Targets the mTOR Pathway to Reverse Autism-Like Phenotypes in Mice. Journal of Neuroscience. 24 January 2018. https://doi.org/10.1523/JNEUROSCI.2010-17.2017
  12. Górecki DC, Beresewicz M, Zabłocka B. Neuroprotective effects of short peptides derived from the Insulin-like growth factor 1. Neurochem Int. 2007 Dec;51(8):451-8. https://pubmed.ncbi.nlm.nih.gov/17582656/
  13. Ramsey MM, Adams MM, Ariwodola OJ, Sonntag WE, Weiner JL. Functional characterization of des-IGF-1 action at excitatory synapses in the CA1 region of rat hippocampus. J Neurophysiol. 2005 Jul;94(1):247-54. https://pubmed.ncbi.nlm.nih.gov/15985695/
  14. Zhao X, McBride BW, Trouten-Radford LM, Burton JH. Effects of insulin-like growth factor-I and its analogues on bovine hydrogen peroxide release by neutrophils and blastogenesis by mononuclear cells. J Endocrinol. 1993 Nov;139(2):259-65. https://pubmed.ncbi.nlm.nih.gov/7508487/
  15. Remacle-Bonnet M, Garrouste F, el Atiq F, Roccabianca M, Marvaldi J, Pommier G. des-(1-3)-IGF-I, an insulin-like growth factor analog used to mimic a potential IGF-II autocrine loop, promotes the differentiation of human colon-carcinoma cells. Int J Cancer. 1992 Dec 2;52(6):910-7. https://pubmed.ncbi.nlm.nih.gov/1281142/
  16. Lemmey AB, Martin AA, Read LC, Tomas FM, Owens PC, Ballard FJ. IGF-I and the truncated analogue des-(1-3)IGF-I enhance growth in rats after gut resection. Am J Physiol. 1991 Feb;260(2 Pt 1):E213-9. https://pubmed.ncbi.nlm.nih.gov/1996625/
  17. Gillespie C, Read LC, Bagley CJ, Ballard FJ. Enhanced potency of truncated insulin-like growth factor-I (des(1-3)IGF-I) relative to IGF-I in lit/lit mice. J Endocrinol. 1990 Dec;127(3):401-5. doi: 10.1677/joe.0.1270401. https://pubmed.ncbi.nlm.nih.gov/2280209/

Dr. Marinov

Dr. Marinov (MD, Ph.D.) is a researcher and chief assistant professor in Preventative Medicine & Public Health. Prior to his professorship, Dr. Marinov practiced preventative, evidence-based medicine with an emphasis on Nutrition and Dietetics. He is widely published in international peer-reviewed scientific journals and specializes in peptide therapy research.

0
    Your Cart
    Your cart is empty