Good Quality Androgen Steroids CAS 118237-47-0 Rad-140 for Bodybuilding
|FOB Price:||US $1 / g|
|Min. Order:||10 g|
|Min. Order||FOB Price|
|10 g||US $1/ g|
|Production Capacity:||500 Tons|
|Transport Package:||1kg/Aluminum Foil Bag or as Your Requirement|
|Payment Terms:||T/T, Western Union, Money Gram|
- Model NO.: 118237-47-0
- CAS No.: 118237-47-0
- Export Markets: Global
- Delivery: 5-7 Working Days Door to Door
- Payment: Western Union, Moneygram, Bank Transfer
- Production Origin: China
- Specification: SGS, ISO9001, KOSHER
- HS Code: 3001
- Product Name: Rad-140
- Appearance: White Powder
- Polciy: Re-Shipping Policy
- Assay: 99%
- Shipping Ways: EMS, TNT, FedEx, DHL, by Air, etc
- Trademark: Network Union
- Origin: China
The possibility of obtaining compounds having tissue-selective activities that are different from that of the endogenous benchmark testosterone might derive from the fact that typical AR receptor activation, which is initiated by the binding of a molecule with affinity for the AR to the AR ligand binding domain, is then followed by a rather remarkable, coordinated series of interactions: These may include a change in receptor topology, dissociation of heat shock proteins, receptor dimerization, receptor phosphorylation, rapid-signaling events, translocation to the nucleus (AR), association with many different coregulatory proteins to form a transcriptional complex that results in the activation or suppression of RNA synthesis from AR-modulated genes, and finally receptor degradation.8 Since each receptorligand complex topology is unique to that ligand structure, one can appreciate that the interaction of any particular ligandreceptor complex with coregulatory proteins is likely to be unique to that ligand as well. Furthermore, because the expression level of AR, the constellation and expression level of coregulatory proteins, and the patterns of post-transcriptional regulatory events differ in each type of androgen target cell, and the topography of AR regulatory sites in the genome differs at each gene, this remarkable choreography of events and interactions provides a rich environment within which one might search for SARMs having a desirable pattern of tissue-selective pharmacology, such as high anabolic but limited androgenic activity.
Further complicating our understanding of the origin of SARM selectivity is the "bio-amplification" of the primary endogenous androgen testosterone. Interestingly, the endogenously produced and very important androgen testosterone serves as a type of "anti-SARM" or "inverse SARM" because its androgenic activity is increased by conversion to the more potent 5α-dihydrotestosterone by the 5α-reductase enzyme in certain tissues including the scalp and prostate (but not in muscle or bone). As a result, androgens that do not undergo such bioamplification in the prostate will demonstrate improved selectivity regarding muscle vs prostate when compared to a testosterone-treated control or an intact animal whose primary endogenous androgen is testosterone.9 More broadly put, one might appreciate that metabolic differences between endogenous androgens such as testosterone or dihydrotestosterone and SARMs can also vouch for at least some selectivity differences.
Our work in the SARM area resulted in the synthesis and evaluation of a large number of candidate templates. While we found it relatively easy to obtain compounds with high affinity for AR, we struggled to achieve compounds that demonstrated good oral efficacy and high in vivo tolerability. After scanning many potential leads for oral, in vivo activity, we arrived at high affinity compound 5 through a combination of synthetic intermediate testing, literature evaluation and fragment combination. We were delighted when 5 demonstrated oral activity in rats.
However, when we performed a pharmacokinetic analysis in rats, we could detect only very low levels of 5 after oral dosing (F < 5%). Further analysis revealed that 5 was efficiently converted to 6in vivo, presumably by cytochromes P450 in the rat liver.10 Compound 6 had similar activity to compound 5in vivo, suggesting that 6was largely responsible for the activity of compound 5.11 An in vitro screen with human microsomes revealed rapid metabolism of compound 5, thus indicating this transformation as a potential human metabolic liability and prompting us to prepare compounds in which the 4′-position of the pendant phenyl was blocked from P450-induced hydroxylation.12 We looked at several analogues containing a 4′-blocking group, and in the course of our efforts we identified compound 7 (RAD140; Figure Figure1)1) as our preclinical development candidate.
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(4).Shipping ways:Ems,Tnt ,Fedex,Dhl,By Air ,etc,
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5a Hydroxy Laxogenin
GW501516 (GW1516 or GSK-516)
Dymethazine DMZ (Mebolazine)
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|Omeprazole||73590-58-6/ 119141-89-8||Benzyl benzoate||120-51-4|
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|Dexamethasone sodium phosphate||55203-24-2/ 312-93-6||Secnidazole||3366-95-8|
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|4 amino-2-Methylpentane citrate (AMP Citrate)||NP|
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