Testolactone

Testolactone is an agent that was primarily used as a medication for breast cancer. It has been discontinued and is no longer available for medical use since 2008.

Here is a detailed breakdown of the information you requested, based on its historical use and known properties:

Testolactone: Detailed Explanation / Different Names

• Detailed Explanation: Testolactone is a synthetic antineoplastic agent (anti-cancer drug) that belongs to the class of steroidal aromatase inhibitors (AIs). It is classified as a first-generation AI.

  • Mechanism of Action: Its principal action is the inhibition of the steroid aromatase enzyme. Aromatase is responsible for converting androgens (like androstenedione) into estrogens (like estrone). By blocking this process, Testolactone reduces the overall level of estrogen in the body. This reduction is beneficial in treating estrogen-dependent breast cancer in postmenopausal women. The inhibition is reported to be noncompetitive and irreversible.

  • Structure: Although structurally related to testosterone, it possesses a six-membered lactone ring in place of the usual five-membered D-ring found in androgen steroids.

• Different Names:

  • Brand Name (US): Teslac

  • Synonyms/Other Names: Fludestrin, Δ-testololactone, 1-dehydrotestololactone, SQ-9538, NSC-23759.

Side Effects and Benefits (Pros and Cons)

Dosage and Frequency

• Recommended Oral Dose (for breast cancer): 250 mg four times a day (totaling 1000 mg/day).

• Frequency: Typically administered multiple times per day (e.g., four times a day).

• Duration: Therapy was recommended to be continued for a minimum of 3 months to properly evaluate the response, unless the disease actively progressed.

Half-Life and Detection Time

Specific, universally cited values for Testolactone's half-life and detection time in the context of sports doping are often difficult to find in standard medical literature, especially since the drug is discontinued.

• Half-Life: A precise elimination half-life is not widely reported in public summaries, but its action as an irreversible aromatase inhibitor means its effect on estrogen synthesis can persist after drug withdrawal as it permanently disables the enzyme.

• Detection Time: Doping detection times for discontinued drugs can be highly variable and depend on the testing method (urine, blood, hair). Information is not standardized, but given its classification as a steroid-derived aromatase inhibitor, detection windows would typically be measured in weeks or months for urine/hair based on the general clearance times for steroid metabolites in competitive sports testing.

Sterogenic, Progestronic, Prolactin Effects, and Anabolic/Androgenic Ratio

• Anabolic Androgenic Ratio:

  • Testolactone is reported to possess some anabolic activity and weak androgenic activity via binding to the androgen receptor (AR).

  • However, its affinity for the AR is very low (e.g., in one study, it showed 0.0029% of the affinity of a potent anabolic steroid like metribolone).

  • The literature emphasizes that it has no in vivo (in the body) androgenic effect in clinical use, as androgenic side effects were rarely (if ever) reported.

  • Given its minimal practical androgenic effect, an official, quantifiable anabolic:androgenic ratio (e.g., 1:10) based on standard clinical tests (like the Hershberger assay) is generally not cited in the same way as for classical anabolic steroids. The practical ratio is considered to be nearly zero or highly skewed away from androgenicity.

• Sterogenic Effects: Testolactone is a steroidal compound, structurally similar to androstenedione/testosterone. Its main action is anti-estrogenic via aromatase inhibition.

• Progestronic Effects: Testolactone is sometimes classified as a progesterone derivative or a progestin in some databases, but its primary clinical mechanism of action is as an aromatase inhibitor and anti-estrogen. The key focus in its therapeutic use was its anti-estrogen action, not progestogenic action.

• Prolactin Effects: No significant hormonal effects other than its anti-estrogen action have been widely reported in clinical studies. There is no standard information indicating a direct or significant effect on prolactin levels.