IGF-1 Des is a naturally occurring analog of insulin-like growth factor 1 (IGF-1) found in the human brain and pig uterine tissues. The difference between the two lies in the length of their amino acid chains. IGF-1 DES is comprised of 67 amino acids and is distinguished by the absence of a tripeptide (consisting of 3 amino acids) at the N-terminus, unlike IGF-1, which contains 70 amino acids in its sequence.

IGF-1 is synthesized by the liver, and it exerts its effect by binding with specific cell surface receptors present on various cells. It is involved in the regulation of growth hormones and promotes cell differentiation and regulation. Further, it stimulates muscle growth and helps build muscle mass. IGF-1 Des is much more potent and bioavailable than IGF-1, which makes it the subject of interest for researchers and scientists. On our website, IGF-1 Des for sale is available for educational and research purposes.

From Pubchem

Synonyms: Insulin-like growth factor 1, des-(1-3)-, Des(1-3)igf-I
Molecular Weight: 7365.4225 g/mol
Molecular Formula: C319H495N91O96S7
CAS Number: 112603-35-7
PubChem CID: 135331146

1. IGF-1 Des and Muscle Health

Research indicates that insulin-like growth factor 1 and IGF-1 Des enhance muscle growth and hypertrophy. Overexpression of IGF-1 in muscles causes an increase in muscle size. A cross-sectional study in women found that low levels of IGF-1 were associated with poor knee extensor muscle strength, slow walking speed, and difficulty with mobility tasks [1].

The activation of the PI3K/Akt signaling pathway by IGF-1 is the possible mechanism through which it promotes muscle building. In one study, researchers found that IGF-1 causes the proliferation of myofibroblast in a dose-dependent manner. Further, they found that insulin-like growth factor 1 influences the myoblasts to enter a new cell cycle and increase the expression of cell cycle-dependent genes. However, the effect was diminished by Inhibitors of PI3k and Akt, indicating that PI3/Akt pathway is important for cell growth induced by IGF-1 [2]. Furthermore, one study reveals that IGF-1-specific muscle expression counteracts muscle wasting caused by angiotensin II [3].

2. IGF-1 Des Potency

The only structural difference between IGF- Des and IGF-1 is the lack of three amino acids at the N-terminus. This minor difference results in the inability of IGF-1 Des to bind with insulin-like growth factor binding proteins (IGFPB) present in plasma and tissues, making it more available for receptors compared to IGF-1. This results in increased bioavailability and potency of IGF-1 Des.

Plus, less affinity of IGF-1 Des to bind with plasma IGFPB results in its increased clearance from the body. This means that the variants that bind poorly to IGFPB have a short duration of action, faster onset of action and rapid withdrawal as compared to IGF-1 [4]

In a study, researchers compared the hypoglycemic effects of IGF-1 and its variant IGF-1 Des in marmosets and pigs. They administered varying doses of test drugs in anaesthetized and conscious animals and measured the blood glucose level over a period of four hours. The results found increased potency of IGF-1 Des (2-3-fold) compared to IGF-1 [5].

Furthermore, one study found that des (1-3) IGF-I administration in 55 kg pigs depressed blood glucose levels with more potency compared to IGF-1 [6].

3. IGF-1 Des and Cognitive Function

IGF-1 plasma concentrations decline with age, and so does cognitive function. Research shows that IGF-1 is associated with improved cognition and neuroprotection. It stimulates cellular processes that promote cell survival, thus protecting neuronal loss [7]. A study found that long-term IGF-1 administration in aged animals increases neurogenesis, vascular density and utilization of glucose in parts of the brain involved in memory and learning [8].

One study determined the actions of IGF-1 in the rat brain and found that it increased excitatory synaptic transmission in CA1 by 40%. It also found that the increased post-synaptic mechanism was due to the involvement of α-amino-3-hydroxyl-5-methyl-4-isoxazolepropionate (AMPA) receptors. Further, it was revealed that the increased synaptic transmission was blocked by PI3k inhibitors, indicating that this effect is dependent on PI3k activation [9].

4. IGF-1 Des and Bone Health

Scientific literature shows that insulin-like growth hormone is a critical mediator of bone health. Research shows that decreased serum IGF-1 is associated with a vertebral fracture in patients with diabetes mellitus, suggesting IGF-1 as a potential marker of vertebral fracture [10].

One study found that IGF-1 and growth hormone administration resulted in increased bone resorption and bone formation. Plus, IGF-1 increased bone healing and showed rapid improvement in patients with Tibia and hip fractures [11].

5. IGF-1 Des and Autism

Deficiency in insulin-like growth factor 1 is associated with social malfunction in children. One study found that IGF-1 levels were significantly lower in children with autism than those without it [12].

Furthermore, it prevented apoptosis and reduced the expression of microRNA (miR-339-5p) that is involved in programmed cell death. It also speculated that the p38 MAPK pathway might be involved in the downregulation of microRNA (miR-339-5p) [9].

IGF-1 is known to improve brain network dysconnectivity, a neurobiological feature of ASD (autism spectrum disorder). Plus, it can also alleviate symptoms of Rett syndrome, having similar characteristics as ASD, in children. This indicates IGF-1 as a potential treatment for disorders like ASD and schizophrenia [13].

In a study, nine children with Phelan-McDermid syndrome (PMS), a type of autism disorder, were enrolled in a randomized double-blind placebo-controlled study. They were given IGF-1 and a placebo for 3 months in random order. The results found the IGF-1 phase to be associated with improvement in social impairment and restrictive behaviors [14].

Summary

IGF-1 Des is a potent natural analog of insulin-like growth hormone. It retains the properties of IGF-1 and is involved in cell differentiation and proliferation. Research shows that it can help build muscle mass and strength. Further, it’s a mediator of bone health and might reverse age-related cognitive decline. At Element Sarms, IGF-1 Des purchase is available for educational and research institutes. Only buy IGF-1 Des if you are a licensed researcher.

1. Cappola, A.R., et al., Association of IGF-I levels with muscle strength and mobility in older women. J Clin Endocrinol Metab, 2001. 86(9): p. 4139-46.
2. Yu, M., et al., Insulin-like growth factor-1 (IGF-1) promotes myoblast proliferation and skeletal muscle growth of embryonic chickens via the PI3K/Akt signalling pathway. Cell Biology International, 2015. 39(8): p. 910-922.
3. Song, Y.-H., et al., Muscle-specific expression of IGF-1 blocks angiotensin II–induced skeletal muscle wasting. The Journal of Clinical Investigation, 2005. 115(2): p. 451-458.
4. Ballard, F.J., et al., Effects of interactions between IGFBPs and IGFs on the plasma clearance and in vivo biological activities of IGFs and IGF analogs. Growth Regul, 1993. 3(1): p. 40-4.
5. Tomas, F.M., P.E. Walton, F.R. Dunshea, and F.J. Ballard, IGF-I variants which bind poorly to IGF-binding proteins show more potent and prolonged hypoglycaemic action than native IGF-I in pigs and marmoset monkeys. J Endocrinol, 1997. 155(2): p. 377-86.
6. Walton, P.E., F.R. Dunshea, and F.J. Ballard, In vivo actions of IGF analogues with poor affinities for IGFBPs: metabolic and growth effects in pigs of different ages and GH responsiveness. Prog Growth Factor Res, 1995. 6(2-4): p. 385-95.
7. Górecki, D.C., M. Beresewicz, and B. Zabłocka, Neuroprotective effects of short peptides derived from the Insulin-like growth factor 1. Neurochem Int, 2007. 51(8): p. 451-8.
8. Sonntag, W.E., M. Ramsey, and C.S. Carter, Growth hormone and insulin-like growth factor-1 (IGF-1) and their influence on cognitive aging. Ageing Research Reviews, 2005. 4(2): p. 195-212.
9. Ramsey, M.M., et al., Functional Characterization of Des-IGF-1 Action at Excitatory Synapses in the CA1 Region of Rat Hippocampus. Journal of Neurophysiology, 2005. 94(1): p. 247-254.
10. Ardawi, M.-S.M., et al., Increased serum sclerostin and decreased serum IGF-1 are associated with vertebral fractures among postmenopausal women with type-2 diabetes. Bone, 2013. 56(2): p. 355-362.
11. Locatelli, V. and V.E. Bianchi, Effect of GH/IGF-1 on Bone Metabolism and Osteoporsosis. Int J Endocrinol, 2014. 2014: p. 235060.