Unique Facets of AAS by Compounds

Author: Type-IIx

Trienes (Δ4,9,11)

Trenbolone: insulin sensitivity, augments muscle satellite cell proliferative response to IGF-I, tissue-level antiglucocorticoid effects (decreased GR number), atherosclerotic and pro-inflammatory (antagonizing MR).

Insulin sensitizing by reducing:

GH pulse amplitude and duration (resulting in decreased serum IGF-I)

PPARγ expression (anti-adipogenic, anti-hyperglycemic), and

TAT activity (analogously to THG: “The Clear”) thereby decreasing gluconeogenesis and hepatic glucose output (lowering blood glucose).

Anabolic effects by increasing the proliferative responsiveness of muscle satellite cells to IGF-I.

Anticatabolic effects by decreasing muscle tissue GR number.

Relative cardiac harm derives from inhibition of cortisol oxidation and exerting MR action, aggravating atherosclerosis via MR activation and inflammatory processes in the vascular endothelium.

Heterocyclically-ringed

Stanozolol (Winstrol): Drying-out effect, long biological half-life.

Mitogenic and myogenic effects by likely increasing free IGF-I bioavailability by decreasing IGFBP-3. [1].

Glucocorticoid modulation by directly, and indirectly via its 16β-hydroxylated metabolite 16β-ST, negatively regulating the LAGS (low affinity glucocorticoid-binding site) in the liver. [2].

Antiprogestagenic effects by antagonizing PR (progesterone receptor). [3].

Profoundly long biological activity (“half-life”) of > 24 h, remarkable among the 17α-alkylated AAS (17AAs). [4].

Joint aching: Stanozolol, notoriously associated with joint pain (“achy, dry joints”) affects synovial fibroblasts, precursors to cells that comprise the synovial joints (e.g., hip, knees, shoulders), by inhibiting DNA synthesis [5], and perhaps secondarily by (particularly potently) stimulating C1-inhibitor (C1-INH) activity [6] – not unique to stanozolol but common to the 17AAs – that might plausibly decrease vascular permeability and affect joint lubrication and delivery of nutrients to joints. [7].

androst-4-ene-3-ones

Fluoxymesterone (Halotestin): [5α-reduction] Particularly reductive of fat mass, systemic antiglucocorticoid effect (competitive inhibition of GR).

Biological half-life of 9.2 h, Usage (Androxy pamphlet) is 10 - 40 mg daily in 1 - 4 doses (Adults).

President JFK was prescribed it for Addison’s Disease (adrenal insufficiency), and his reputation for sexual potency was legendary.

Both the 11β-hydroxyl & 9α-fluoro group are known to increase binding to the glucocorticoid receptor (GR).

competitive 11β-HSD2 inhibition, while increasing serum & free cortisolwhich converts cortisone to its more active metabolite cortisol. The addition of the 9-fluoro group would likely increase its affinity for that enzyme as well, since it bends the A-ring of the steroid to the α-side,, ,,, resulting in a more glucocorticoid like structure. Most atypical among the AAS structurally! More glucocorticoid-like. Even estradiol is more androgen-like than this!

JFK prescribed it for Addison’s Disease

Trestolone (MENT): [aromatization] Particularly suppressive (decreased LH, FSH).

Testosterone: [aromatization & 5α-reduction] Bioidentical.

Nandrolone (Deca durabolin; NPP): [aromatization & 5α-reduction] Joint benefits (increased type I collagen deposition), depression and learning, memory deficits (increased homovanillic acid).

5α-androstan-3-ones

Oxandrolone (Anavar): A 2-oxasteroid. Particularly lipolytic, enhances hepatic ketosis.

Methasterone (Superdrol): 2α-methylation dramatically increases anabolic and reduces androgenic potency, most toxic commercially available AAS (resistant to metabolism & potent 17AA).

1-enes (androst-1-ene-3-ones)

1-Testosterone (Dihydroboldenone): Increases DHT (perhaps via 17β-HSD1 inhibition but not 5α-reduction), increases C-reactive protein either directly or by requiring guaiacol to hold in solution.

1,4-dienes (androsta-1,4-dienes)

Metandienone (Dianabol): [aromatizable] Decreases ACTH (antiglucocorticoid effect), potently suppressive, potently hematopoeitic.

2-enes (no 3-keto group)

Epistane: highly unusually lacking the 3-keto group (for which the O atom has a lone pair of electrons allowing its action as a H-bond acceptor, able to interact with polar or charged amino acids to form strong bond with the N-terminus/amino-group), acts partly as a prodrug to desoxymethltestosterone (Madol), potently antigynecomastic.