Dianabol For Sale: Effectivity And Regulation

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Class & Structure: www.bidbarg.com Synthetic anabolic‑androgenic steroid (AAS) derived from testosterone; contains a 17α‑methyl group and an additional 4‑methyl group, giving it a.

Dianabol For Sale: Effectivity And Regulation


Dianabol (Methandrostenolone)

  • Class & Structure: Synthetic anabolic‑androgenic steroid (AAS) derived from testosterone; contains a 17α‑methyl group and an additional 4‑methyl group, giving it a "double‑bumped" shape.

  • Administration: Oral tablets (commonly 2–6 mg once or twice daily). The oral route requires hepatic metabolism, so it is hepatotoxic at higher doses.

  • Half‑life & Action: ~12 h; peaks in the bloodstream within a few hours after ingestion.

  • Effects: Strong anabolic activity with moderate androgenic potency. Rapid muscle mass gain, increased strength, and www.bidbarg.com early improvements in performance (especially when combined with other compounds).

  • Side‑effects: Liver strain or damage (especially at doses >6 mg/day), mild water retention, possible acne, mood swings. Rarely causes virilization in women.





2. What is "the difference" between S4 and S4‑P?









FeatureS4S4‑P
StructureStandard 17α‑acetylated, 3‑hydroxyl steroid (like many anabolic steroids).Contains a progestin‑type group at the C3 position: an "oxo‑" or "enone" system that makes it more progestogenic.
Progestogenic activityMinimal – primarily acts through androgen receptors.High – behaves much like a synthetic progesterone (e.g., medroxyprogesterone).
MetabolismRapidly cleared, mainly via 3‑oxidation and conjugation.More resistant to metabolism; longer half‑life due to steric hindrance at C3.
Side‑effectsCan cause gynecomastia if testosterone levels rise (via aromatase).Additional side‑effects: mood swings, water retention, nausea, increased appetite, weight gain.
Typical dosage0.5–1 mg daily for acne or hair loss; may be combined with minoxidil.0.25–0.75 mg daily (often in divided doses) to reduce side‑effects; usually taken at night.

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How the Body Processes the Two Forms









StepNormal TestosteroneC3‑Modified Testosterone
SynthesisEndogenous production in Leydig cells of testes or adrenal cortex (in men).Exogenously supplied; does not require conversion.
Transport99 % bound to SHBG and albumin → very low free fraction.Same binding profile; the same proportion is "free" but due to the chemical change the free hormone may be less able to cross cell membranes.
Cellular UptakeDiffuses through lipid bilayer into cells where it binds androgen receptors (AR).Diffusion significantly reduced; the molecule’s altered polarity and steric hindrance limit passive entry, especially in tissues with low lipid content.
MetabolismRapid 5α‑reduction by 5α‑reductase → DHT → potent AR activation; further conjugation & excretion.The bulky group may inhibit 5α‑reductase recognition; less conversion to DHT. Conjugation may also be altered, potentially increasing renal clearance or hepatic uptake.
Target Tissue EffectHigh concentration in prostate, skin, hair follicles → pronounced androgenic effects (growth, hyperplasia).Lower penetration leads to reduced stimulation of androgen‑dependent tissues; systemic side‑effects like gynecomastia or acne may diminish due to lower bioavailability at target sites.

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5. Predicted Pharmacological Profile











PropertyLikely Value
Molecular weight~450 Da (within drug‑like range)
LogP~3–4 (balanced lipophilicity)
Topological polar surface area (tPSA)70–90 Ų (moderate, allows membrane crossing)
Oral bioavailabilityModerate; may require formulation to improve absorption
Half‑life~12–24 h (due to moderate lipophilicity and metabolic stability)
Metabolic pathwayPhase I oxidation of the side chain; phase II conjugation of the phenolic OH
Toxicity profileLower acute toxicity compared to 3,4‑DMP; hepatotoxicity risk remains but reduced

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Conclusion



The designed compound, 2‑(1‑(pyridin‑3‑yl)ethyl)oxyphenol, strategically incorporates a pyridine ring for improved solubility and a phenolic hydroxyl group to reduce metabolic liability. These structural changes are expected to:


Lower acute toxicity relative to 3,4‑DMP.
Maintain or improve the ability to permeate biological membranes (due to the aromatic system).

  • Retain an acceptable degree of lipophilicity for cell penetration while enhancing aqueous solubility.


While this design is rational and grounded in structure–activity relationships, experimental validation—cytotoxicity assays, metabolic stability studies, and pharmacokinetic profiling—would be necessary to confirm its safety profile. Nonetheless, the proposed molecule represents a promising candidate for further toxicological investigation.
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