RAMATROBAN: Highly Selective PGD2 Receptor Antagonist 3mg/ml, 60ml
Ramatroban is a PGD2 receptor antagonist, also called a GPR-44 receptor antagonist, CRTH2 receptor antagonist, or true PGD2 blocker. Unlike other types of PGD2 inhibitors, ramatroban prevents all activity at the PGD2 receptor from both prostaglandin D2 and 15PGJ2, but does not interfere with the activity of other prostaglandins such as PGE2 or PGF2a. Due to a proven safety record and clinical history, in the future ramatroban may be one of the first true PGD2 inhibitors to be marketed for treatment of baldness.
In 2012 a research breakthrough in the field of androgenic alopecia and male pattern baldness, contained within a study by Garza, Cotsarelis, et al, identified a compelling new chemical pathway in murine and human baldness. Although previous androgenic alopecia hypotheses, such as presence of androgens (DHT) in the scalp, appeared to partially explain male pattern baldness, even taking into account individual genetic differences they did not account for mixed success of treatments such as finasteride and dutasteride, nor explain the local mechanisms of DHT in the scalp in a detailed or satisfactory way.
Prostaglandin D-synthase or PGDS is an enzyme that has been shown to convert arachidonic acid (AA) into prostaglandin (PGs). Inhibitors of PGD-synthase are one promising way of targeting the PGD2 baldness pathway, but ramatroban represents a more direct approach to inhibit PGD2, and is proven to be effective in inflammatory and immune disorders.
The Garza 2012 research not only implicates the arachidonic acid (AA)/prostaglandin (PG) pathway, it reframes androgenic alopecia as an inflammatory/immune disorder. Previously published papers such as this one from 2002, published in Experimental Gerontology, contained speculation on molecular mechanisms such as inflammatory reactions that could explain the lack of long-term efficacy of DHT-inhibiting anti-androgens and 5-AR-inhibitors:
Since the clinical success rate of treatment of AGA with modulators of androgen metabolism or hair growth promoters is limited, sustained microscopic follicular inflammation with connective tissue remodeling, eventually resulting in permanent hair loss, is considered a possible cofactor in the complex etiology of AGA. 
Though the role of PGD2 in male pattern baldness in humans and rats was a new discovery, PGD2 and its downstream metabolite 15-dPGJ2 had been previously implicated in allergic and inflammatory reactions elsewhere in the body. The specific prostaglandin receptor now implicated in baldness, known as GPR-44, CRTH2, or DP2, is also a target for anti-allergy therapies that, when blocked or antagonized, effectively reduces allergic symptoms in experimental models:
PGD2, produced by mast cells, has been detected in high concentrations at sites of allergic . It can stimulate vascular and other inflammatory responses by interaction with D prostanoid receptor (DP) and chemoattractant receptor-like molecule expressed on Th2 cells (CRTH2) receptors. A significant role for PGD2 in mediating allergic responses has been suggested based on the observation that enhanced eosinophilic lung and cytokine production is apparent in the allergen-challenged airways… PGD2 preferentially up-regulates proinflammatory cytokine production in human Th2 cells through a CRTH2-dependent mechanism in the absence of any other costimulation and highlight the potential utility of CRTH2 antagonists in the treatment of allergic diseases.
The media quickly picked up on the research and also pointed out that existing allergy drugs may be candidate drugs for PGD2 baldness cures, or for development of similar drug analogs that could cure male pattern baldness soon:
Researchers at the Univ. of Pennsylvania say they have identified the scalp chemical that stops hair from growing, and believe it may finally—finally!—lead to the elusive cure for male pattern baldness.
The scientists found that a protein called PDG2 was three times as prevalent on the scalps of balding men. (PDG2-blocking drugs are already being tested by researchers working on alternative treatments for asthma, so they're hopeful testing for baldness can be expedited.) The news was met with joy in England, where an estimated 7.4 million men are bald or balding. "Excitingly," the Daily Mail reported, "drugs that block the protein have already been developed for other purposes, meaning a hair restoring lotion or potion could be on the market in under five years." (http://news.yahoo.com/blogs/sideshow/cure-baldness-researchers-identify-scalp-chemical-stops-hair-143906562.html)
In Molecular Pharmacology a 1% (v/v) solution of ramatroban in DMSO was found to completely inhibit a CRTH2 receptor activity; the authors expressed optimism at the usefulness of ramatroban for further in vitro and ex vivo studies:
Such biased antagonists may serve as valuable tools for dissecting the contribution of individual signaling pathways of receptors in physiological and pathophysiological processes in vitro and ex vivo.
A brief review of the Garza and Cotsarelis data from 2012 elucidates the CRTH2 as a key receptor signaling pathway in human baldness:
prostaglandin D(2) (PGD(2)), is similarly elevated in bald scalp. During normal follicle cycling in mice, Ptgds and PGD(2) levels increase immediately preceding the regression phase, suggesting an inhibitory effect on hair growth. We show that PGD(2) inhibits hair growth in explanted human hair follicles and when applied topically to mice. Hair growth inhibition requires the PGD(2) receptor G protein (heterotrimeric guanine nucleotide)-coupled receptor 44 (GPR44), but not the PGD(2) receptor 1 (PTGDR). 
Ramatroban is a promising candidate drug for future research into male pattern baldness treatments due to its potent binding to the CRTH2 receptor; it binds strongly enough to inhibit PGD2 receptor activity while in the same solution as potent PGD2 receptor agonists (activators), even 15-dPGJ2, which is 15 times more powerful than PGD2:
We previously showed that ramatroban (Baynastrade mark), a thromboxane A(2)(TxA(2)) antagonist, had inhibited prostaglandin D(2)(PGD(2))-stimulated human eosinophil migration mediated through activation of chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2). However, detailed pharmacological characterization of its inhibitory activity has not been described. In the present study, we showed that [(3)H]ramatroban bound to a single receptor site on CRTH2 transfectants with a similar K(d) value (7.2 nM) to a TxA(2) receptor (8.7 nM). We also demonstrated that ramatroban inhibited PGD(2)-, 15-deoxy-Delta(12, 14)-PGJ(2)(15d-PGJ(2))- and indomethacin-induced calcium responses on CRTH2 transfectants in a competitive manner with similar pA(2) values (8.5, 8.5, and 8.6, respectively). This is the first report showing the evidence for direct binding of ramatroban to CRTH2, revealing its competitive inhibitory effects and another interesting finding that PGD(2), indomethacin and 15d-PGJ(2) share the same binding site with ramatroban on CRTH2.
 Garza LA, Liu Y, Yang Z, Alagesan B, Lawson JA, Norberg SM, Loy DE, Zhao T, Blatt HB, Stanton DC, Carrasco L, Ahluwalia G, Fischer SM, FitzGerald GA, Cotsarelis G. Prostaglandin D2 inhibits hair growth and is elevated in bald scalp of men with androgenetic alopecia. Sci Transl Med. 2012 Mar 21;4(126):126ra34.
 Trüeb RM. Molecular mechanisms of androgenetic alopecia. Exp Gerontol. 2002 Aug-Sep;37(8-9):981-90.
 Xue L, Gyles SL, Wettey FR, Gazi L, Townsend E, Hunter MG, Pettipher R. Prostaglandin D2 causes preferential induction of proinflammatory Th2 cytokine production through an action on chemoattractant receptor-like molecule expressed on Th2 cells. J Immunol. 2005 Nov 15;175(10):6531-6.
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 Sugimoto H, Shichijo M, Okano M, Bacon KB. CRTH2-specific binding characteristics of [3H]ramatroban and its effects on PGD2-, 15-deoxy-Delta12, 14-PGJ2- and indomethacin-induced agonist responses. Eur J Pharmacol. 2005 Nov 7;524 (1-3):30-7 16256979
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