Cure found for acne, scientists claim reduces sebum by 90%

indie85

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Found this on HLH, thought it may be pretty significant...
Scientists believe they have found a breakthrough treatment for acne.
They claim that the drug, SMT D002, can reduce the flow of sebum - an oily substance produced by the skin and believed to be a significant cause - by 90 per cent.

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At present, the drug is in pill form and is used to treat a condition other than acne but a pharmaceutical company plans to turn it into a cream for easier use.

Researchers believe it could become as effective a treatment as retinoic acid - a form of vitamin A - which is currently used to treat moderate to severe cases.

However, Roaccutane, the most widely used formulation of retinoic acid, has been linked to suicides among acne sufferers.

SMT D002 produced no significant side-effects when volunteers took it in pill form. Around three in every 10 patients taking retinoic acid do not respond to the drug, leaving many sufferers without an effective treatment.

Richard Pye, of Summit Corporation, based in Oxford, said the company was turning the drug into a cream because it was likely to work more quickly.

For commercial reasons Summit would not reveal the name of the existing drug form that they are developing their new acne treatment.

Richard Storer, the company's chief scientist, said: "It is a major drug, but we cannot reveal its name or the condition it currently treats."
http://www.telegraph.co.uk/news/main.jh ... lth417.xml

Damn thats a pretty huge reduction, if only they let us know what damn compound it is, its obviously widely available already...
 

abcdefg

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I guess if that happens we will find out if sebum really is a major factor in hairloss if that treatment ever happens. Maybe science will figure out the relationship between sebum, dht, acne, and all this other crap we just guess at right now.
 

harold

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abcdefg said:
I guess if that happens we will find out if sebum really is a major factor in hairloss if that treatment ever happens. Maybe science will figure out the relationship between sebum, dht, acne, and all this other crap we just guess at right now.

I thought this was a great recent study. seems DHT needs linoleic acid (or something similar ie a PPAR ligand) to cause increased sebum production and linoleic acid in turn causes the production of DHT from testosterone to go through the roof.
hh

Br J Dermatol. 2007 Mar;156(3):428-32.Links
Testosterone metabolism to 5alpha-dihydrotestosterone and synthesis of sebaceous lipids is regulated by the peroxisome proliferator-activated receptor ligand linoleic acid in human sebocytes.
Makrantonaki E, Zouboulis CC.

Laboratory of Biogerontology, Dermatopharmacology and Dermatoendocrinology, Institute of Clinical Pharmacology and Toxicology, Charité University Medicine Berlin, Berlin, Germany.

BACKGROUND: Despite the clinical evidence that androgens stimulate sebaceous lipids, androgens in vitro have shown no similar effects. This contradiction led to the assumption that cofactors may be required for lipid regulation and peroxisome proliferator-activated receptor (PPAR) ligands were suggested to be adequate candidates. OBJECTIVES: The influence of testosterone and linoleic acid, a PPAR ligand, as single agents and in combination with of LY191704, a 5alpha-reductase type I inhibitor, was examined on 5alpha-dihydrotestosterone (5alpha-DHT) synthesis and lipid content in human SZ95 sebocytes. METHODS: Cell proliferation and viability were measured by the 4-methylumbelliferyl heptanoate fluorescence assay and by the Boehringer Lactate Dehydrogenase Assay kit, respectively. 5alpha-DHT enzyme-linked immunosorbent assay was used for the detection of 5alpha-DHT synthesis in cell supernatants after treatment, whereas lipid production was documented by means of the Nile red lipid microassay and fluorescence microscopy. RESULTS:Testosterone promoted 5alpha-DHT synthesis (P < 0.001), whereas linoleic acid increased sebaceous lipids (P < 0.001). The combination of testosterone and linoleic acid exhibited a synergistic effect on the synthesis of 5alpha-DHT (P < 0.01 vs. testosterone) and sebaceous lipids (P < 0.01 vs. linoleic acid). Furthermore, LY191704 reduced 5alpha-DHT and sebaceous lipid levels (P < 0.01 and P < 0.001 in comparison with testosterone/linoleic acid, respectively). Cell proliferation and viability remained unchanged under treatment with all compounds tested. CONCLUSIONS: These data suggest a catalytic effect of PPAR ligands on cellular testosterone activation by 5alpha-reduction and the importance of the latter for the regulation of sebaceous lipids.
 
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