Talk:Insulin-like growth factor 1

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Untitled[edit]

What about IGF-2? can somebody elaborate on this?

IGF-2 is a naturally occuring second protein, related to MGM-1. It binds the IGF1 receptor at somewhat lower affinity than IGF1. Both IGF1 and IGF2 can induce growth in the animal via the IGF1 receptor. Gacggt 21:46, 26 July 2006 (UTC)


long r3 igf-1[edit]

The most effective (artifically modified) form of IGF is Long R3 IGF-1, it has been chemically altered and has had amino acid changes which cause it to avoid binding to proteins in the human body and allow it to have a much longer half life, around 20-30 hours. “Long R3 IGF-1 is an 83 amino acid analog of IGF-1 comprising the complete human IGF-1 sequence with the substition of an Arg(R) for the Glu(E) at position three, hence R3, and a 13 amino acid extension peptide at the N terminus. This analog of IGF-1 has been produced with the purpose of increasing the biological activity of the IGF peptide.” The only two IGF-1 Long R3 brands available on the market today are Revitropin and Igtropin. There is also a [[black market] for it with an average price of $150/1mg. This black market is especially used by [bodybuilders] and [athletes] who want to increase their lean body mass.

I removed the above temporarily for a couple of reasons. The reader will think this is simply another tested and approved IGF1 or somatropin product when it is deliberately being marketed as an "offshore" pharmaceutical for "experimental" use, which in plain language means they have not demonstrated efficacy or safety to any qualified agency, and they want to sell it without oversight, without liability or legal recourse for the buyer. This needs to be made excruciatinly clear. For those who mistrust "Big Pharma" the only thing potentially worse is a situation like this. The second problem is that statements about the effectiveness of a product like this need references. If there are no published papers about this compound, it does not belong here. Thanks for understanding. alteripse 01:01, 14 May 2006 (UTC)


IGF-1 and lifespan[edit]

I've heard that IGF-1 also interacts with lifespan; invertebrates with deficient IGF-1 receptors have a longer lifespan. However, low levels of IGF-1 in older human adults seems is linked with a shorter lifespan. —The preceding unsigned comment was added by Bayle Shanks (talkcontribs) 04:29, 12 December 2006 (UTC).

See for example http://dx.doi.org/10.1007/s00018-004-4297-y Bayle Shanks 04:31, 12 December 2006 (UTC)

There is indeed some record of increased lifespan in the (partial) absence of IGF-1 receptors (and consequently: reduced IGF-1 signaling). [Paper: IGF-1 receptor regulates lifespan and resistance to oxidative stress in mice.]. You have to see the bigger picture as well however, increased life-span doesn't mean staying young, nor does it mean that there are no other harmfull effects, this particular article only addresses life-span & resistance to oxidative stress in mice. Mice are quite different from men, they are short-lived high breeders (high predator pressure), while we are long-lived, slow breeders. Mechanisms that influence lifespan can thus be expected to have different effects in mice versus humans. Daviddecraene 08:03, 12 December 2006 (UTC)

Recent evidence suggests caloric restriction doesn't in humans doesn't lower IGF-1 as it does in mice (longer lifespan), however, protein restriction DOES do this. Somebody should add a bit on IGF-1 and lifespan. http://www.physorg.com/news141484846.html 210.215.140.180 (talk) 10:09, 25 September 2008 (UTC)

Insulin binds to IGF-IR[edit]

While the article mentions that IGF-I binds to the insulin receptor, it doesn't mention anywhere that insulin binds to IGF-IR. This is of vital importance to, for example, the development of recombinant insulin analogs, since high IGF-I is correlated with breast cancer and diabetic retinopathy. A10Asp, for example, causes cancer in mice and shows 20x IGF-IR affinity. Glargine also shows 6-8x affinity in vitro, which is part of the worry about a possible (though unlikely) link to breast cancer. I can write this and gather some references, but if anybody else feels bold in the meantime, it needs to be added. Eebster the Great (talk) 17:02, 13 July 2009 (UTC)

Insm[edit]

I feel like this is a slanted position:

Insmed was found to infringe on patents licensed by Tercica, which then sought to get a U.S. district court judge to ban sales of Iplex. [3] To settle patent infringement charges and resolve all litigation between the two companies, Insmed in March 2007 agreed to withdraw Iplex from the U.S. market, leaving Tercica's Increlex as the sole version of IGF-1 available in the United States. [4]

This doesn't seem to be true according to [drugs.com[1]]

Through licensing and development rights granted by Tercica and Genentech, Insmed will have freedom to operate regarding the manufacture, development and commercialization of IPLEX for certain non-short stature indications including severe insulin resistance, myotonic muscular dystrophy and HIV associated adipose redistribution syndrome (HARS), subject to opt-in rights and royalty provisions for Tercica and Genentech.

It goes on to discuss the terms of the agreement including opt-in for indications genetech and tercica find appealing, though tercica isn't an independent company any longer to my knowledge. I'm not necessarily the authority on this though. I thought others might have input.

for disclosure I own stock in insm otherwise wouldn't have stumbled onto this. —Preceding unsigned comment added by Lycanter (talkcontribs) 05:35, 28 March 2010 (UTC)


This belongs not directly to Insmed, but to the statement "Also, since IGFBP-3 has a lower affinity for IGF-1 than IGF-1 has for its receptor, IGFR, its binding does not interfere with IGF-1 function". In my opinion and also in the opinion of other autors IGFBP-3 binding affinity for IGF-1 is much higher than the affinity between IGF-1 and it's receptor. Please have a look at "The Insulin-Like Growth Factor-Binding Protein (IGFBP) Superfamily1" (Vivian Hwa, Youngman Oh and Ron G. Rosenfeld; Endocrine Reviews 20 (6): 761-787) and "Biosensor measurement of the interaction kinetics between insulin-like growth factors and their binding proteins" (Wong, M. S. Fong, C. C., Yang, M.; Biochimica et Biophysica Acta 1432 (1999) 293^301) —Preceding unsigned comment added by 217.111.75.13 (talk) 14:42, 6 October 2010 (UTC)

Causes or is raised by cancers[edit]

Article says "Several studies have shown that increased levels of IGF lead to an increased risk of cancer." with no source, but in some cases the raised IGF(-1) is caused by the cancer (generated within the cancer cells) rather than the IGF causing the cancer. Need a RS. Maybe The role of the IGF system in cancer growth and metastasis: overview and recent insights. 2006 Rod57 (talk) 17:23, 24 November 2010 (UTC)

Deer Antler extract (Deer antler velvet?)[edit]

It's becoming very big in the news about IGF-1 and Deer Antler velvet. A few things I'm interested in: 1.) Is the Deer Antler IGF-1 the same as the Insulin-like growth factor 1? 2.) Can IGF-1 be taken orally like all the supplements online say? Many growth factors get destroyed in the stomach, and that's why the oral-route isn't acceptable. This leads me to the bigger question "what peer-reviewed research gives us details on Deer antler velvet?" —Preceding unsigned comment added by 67.222.112.250 (talk) 17:44, 21 January 2011 (UTC)

Ecuadorian study[edit]

Here's the NYT story on the Ecuadorian study of Laron syndrome by Dr. Jaime Guevara-Aguirre Ecuadorean Villagers May Hold Secret to Longevity By NICHOLAS WADE.

Primary source is Science Translational Medicine, http://stm.sciencemag.org/content/3/70/70ra13.abstract but that's behind a paywall. --Nbauman (talk) 14:21, 17 February 2011 (UTC)

molecular weight of IGF-1[edit]

The MW listed in the main article for IGF-1 is incorrect. The correct value is 7649 Daltons. Reference article: Rinderknecht & Humbel, J. Biolog Chem, col 253, no. 8, pp 2769-2776, 1978. — Preceding unsigned comment added by 66.57.33.243 (talk) 13:14, 6 January 2013 (UTC)