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Savic, M.P.; Kuzminac, I.Z.; Nikolic, A.R. Medicinal Uses and Benefits of Testolactone. Encyclopedia. Available online: https://encyclopedia.pub/entry/43180 (accessed on 08 February 2026).
Savic MP, Kuzminac IZ, Nikolic AR. Medicinal Uses and Benefits of Testolactone. Encyclopedia. Available at: https://encyclopedia.pub/entry/43180. Accessed February 08, 2026.
Savic, Marina P., Ivana Z. Kuzminac, Andrea R. Nikolic. "Medicinal Uses and Benefits of Testolactone" Encyclopedia, https://encyclopedia.pub/entry/43180 (accessed February 08, 2026).
Savic, M.P., Kuzminac, I.Z., & Nikolic, A.R. (2023, April 18). Medicinal Uses and Benefits of Testolactone. In Encyclopedia. https://encyclopedia.pub/entry/43180
Savic, Marina P., et al. "Medicinal Uses and Benefits of Testolactone." Encyclopedia. Web. 18 April, 2023.
Medicinal Uses and Benefits of Testolactone
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This entry is adapted from the peer-reviewed paper 10.3390/ddc2010005

Testolactone is structurally related to testosterone and belongs to the first generation of aromatase inhibitors. It is a non-selective irreversible aromatase enzyme inhibitor that was one of the first steroids used in the clinical treatment of breast cancer. 

teslac aromatase inhibitor breast cancer testolactone

1. Cancer

1.1. Breast Cancer

One of the first papers on the use of testolactone for the treatment of breast cancer was published in 1960 by Segaloff et al. [1]. In their research, they observed sustained objective remission of the advancing breast cancer. In addition to the effectiveness of parenteral therapy with testolactone, later in their work, they investigated the efficacy of the oral administration of this agent, where testolactone caused a higher response rate in oophorectomy failures than other hormonal agents, with objective regression of disease, and increase in excretion on 17-ketosteroids, and no evidence of androgenicity [2]. Further investigations were conducted by Cantino et al. [3] when they increased the dose of testolactone in an attempt to obtain better control of the disease, but without improvement in the objective regression rate.
In order to develop potent anticancer agents, The National Cancer Institute has been working with the Cooperative Breast Cancer Group since 1957. For that reason, Goldenberg performed clinical studies in which breast cancer was treated with testolactone, medroxyprogesterone acetate, or oxylone acetate, where testolactone produced the lowest objective remissions, while the observed survival experience was the best for the patients receiving testolactone and poorest for those receiving medroxyprogesterone acetate [4]. In further study of advanced breast cancer in women, Goldenberg et al. [5] applied testolactone as a reference substance to confirm the biological activity of calusterone. In their research, a randomized clinical trial of calusterone and testolactone produced objective remissions of advanced breast cancer in 28% of women receiving calusterone and 18% of those given testolactone. In the next report of the Cooperative Breast Cancer Group, Goldenberg et al. [6] described a clinical trial of aromatase inhibitor and antimetabolite therapy for advanced female breast cancer, where an objective regression rate of 20% was achieved in women receiving oral testolactone, 6% in patients given intravenous fluorouracil alone, and 14% when they were administered together.
Barone et al. [7] examined postmenopausal women with metastatic breast cancer on oral therapy with testolactone. Based on measuring the levels of estrone, serum androstenedione, and testosterone, they came to the conclusion that testolactone is a potent inhibitor of peripheral aromatization of androstenedione into estrone, without affecting serum androstenedione and testosterone levels. In further in vitro studies it was determined that estrogen formation can be blocked directly at the tumor site and in addition to reducing of the level of plasma estrone, estradiol was lowered [8]; moreover, testolactone can block peripheral formation of estrogens in breast tumors [9]. Further, Kaufman [10] analyzed the impact of estrogen, progestin, androgens, corticosteroids, and testolactone in combination with non-hormonal therapy for the treatment of breast cancer, and pointed out that additive hormonal therapy still has a major role in the management of the advanced breast cancer patient.

1.2. Prostatic Carcinoma

The treatment of hormone-dependent prostate cancer, aiming at reducing circulating androgen levels, mainly estrogen administration, gained popularity in the 1980s of the last century. The mechanisms behind the beneficial effects of estrogens on prostatic carcinoma were not yet known. In order to investigate the role of estrogens in human male endocrinology Leinonen et al. [11] performed a study where tamoxifen or testolactone was given to prostatic carcinoma patients, concluding that in vivo contribution by testolactone or its metabolites was very small.

1.3. Human Benign Prostatic Hyperplasia (BPH)

Testolactone was applied for endocrine treatment of benign prostatic hyperplasia (BPH), since there was an assumption that estrogens might also be causally related to the onset and maintenance of BPH. This approach was defined by Schweikert and Tunn [12], because at that time it was known that, among other, peripheral aromatization of circulating androgens is the major source of estrogen in men, and the amount of aromatized androgens increases with advancing age. While, aromatization of androstenedione to estrone has the highest conversion rates in cells derived from BPH tissue, authors have used testolactone for endocrine treatment of benign prostatic hyperplasia (BPH) in thirteen patients. As a result, prostatic volume decreased.
In further studies of BPH, Bartsch et al. [13] investigated the presence of aromatase in benign prostatic hyperplasia and possible inhibition of the enzyme 17β-hydroxysteroid dehydrogenase (17βHSDH). Bartsch et al. [13] have investigated whether aromatase inhibiting compounds might partially act by inhibition of 17βHSDH, but beneficial effects of testolactone observed in BPH patients were due to inhibition of aromatase and not of 17βHSDH.

1.4. Desmoid Tumors

The use of testolactone in the treatment of desmoid tumors is also described in the literature. Considering that there was an assumption that these tumors were hormone dependent, and additionally, estrogen receptors have been found in 33 to 75% of the desmoid tumors, the idea of using aromatase inhibitors in their treatment arose [14]. Research by Waddell [15] concerns the chemical treatment of desmoid tumors with testolactone and subsequently with theophylline and chlorothiazide. These compounds are inhibitors of cyclic adenosine monophosphate (cAMP) phosphodiesterase (PDE), which is known to have in vitro effects on tumor cells, while testolactone by itself has some inhibitory effect on cAMP phosphodiesterase. The authors have concluded that the combination of these three drugs synergize the action of 3’,5’-adenosine monophosphate and the latter two may work by inhibiting the action of 3’,5’-adenosine monophosphate diesterase. Waddell and Kirsch [16] in their further research have investigated combination therapy regimens consisting of steroidal aromatase inhibitor (testolactone) and nonsteroidal anti-inflammatory drugs (indomethacin, sulindac, warfarin and vitamin K1). Their therapeutic recommendations minimized the effects of estrogen and inhibited prostaglandin and cAMP synthesis, which have influence on growth and proliferation of fibroblasts. Furthermore, Gansar and Krementz [17] published a case of a patient with a desmoid tumor, which was treated with testolactone and chlorothiazide, where a marked decrease in pain was reported, along with a change in the shape of the lesions.
Tsukada et al. [14] investigated noncytotoxic drug therapy for the treatment of intra-abdominal desmoid tumors in patients with familial adenomatous polyposis (FAP). They have concluded that for female patients, tamoxifen may be used, and in male patients intolerant of NSAIDs, progesterone or testolactone may have some effect.

1.5. Carcinoma of the Pancreas

The results of two chemotherapy regimens for inoperable carcinoma of the pancreas have been described. One group was treated with 5-fluorouracil and coumadin, while the other was treated with 5-fluorouracil and testolactone or spironolactone. The authors have concluded that testolactone has no significant additive benefits in prolonging survival in combination treatment programs [18][19][20].

2. Precocious Puberty

If a boy develops secondary sexual characteristics before the age of 9 years or a girl before the age of 8 years, the child is considered to have sexual precocity. They can be classified into variations of normal pubertal development, and contrasexual pubertal development: central precocious puberty (CPP), which results from early activation of the hypothalamic–pituitary–gonadal axis; or peripheral precocious puberty (PPP), which appears due to extrapituitary gonadotrophin secretion or independent sex steroid secretion [21][22]. Further, familial male-limited precocious puberty (FMPP), is caused by a mutation in the luteinizing hormone/chorionic gonadotropin receptor gene, resulting in the receptor being constitutively activated, which causes excessive production of testosterone [23]. In order to mitigate the effects of estrogen on growth, skeletal maturation, and secondary sexual development, aromatase inhibitors began to be used in the mid-1980s. In the treatment of selective forms of precocious puberty, testolactone has been demonstrated to be tolerable and effective, while diverse results with testolactone have been achieved in girls with McCune–Albright syndrome [24].
In their research, Laue et al. [25] hypothesized that the blockade of androgen action and estrogen synthesis would normalize the growth of boys with familial male-limited precocious puberty (FMPP) because puberty in boys appears to be mediated by both androgens and estrogens. To test this hypothesis, authors studied nine boys during treatment with an antiandrogen (spironolactone) or an inhibitor of aromatase (testolactone), followed by treatment with both agents. Only a combination of spironolactone and testolactone, given for at least six months, restored both the growth rate and the rate of bone maturation to normal prepubertal levels and controlled acne, spontaneous erections, and aggressive behavior. Blockade of both androgen action and estrogen synthesis is an effective short-term treatment for familial male precocious puberty. While FMPP is a luteinizing-hormone-releasing hormone-independent (LHRH-independent) form of precocious puberty, in the continuation of their research, Laue et al. [26] have included testolactone and spironolactone in the therapy with LHRH agonist deslorelin, which have been effective as single agents in the treatment of LHRH-dependent precocious puberty. Combined therapy decreased peak LH, plasma testosterone, bone maturation rate, and growth velocity. They have concluded that the rise in gonadotropin levels during central activation of hypothalamic LHRH secretion in boys with familial male-limited precocious causes a partial escape from the combined effect of spironolactone and testolactone. The addition of deslorelin to the combined therapy appears to restore the control of puberty in this setting.
In their work Cummings et al. [27] examined whether elevations in testosterone and androstenedione recorded during treatment in FMPP were caused by interference of testolactone and spironolactone in radioimmunoassays. They measured serum levels of testosterone and androstenedione serially by RIA for 24 h in a girl with McCune–Albright syndrome, a boy with familial male precocious puberty, and in a healthy postmenopausal control after a single oral dose of testolactone. They have concluded that testolactone significantly interferes in these serum RIAs, making their use unreliable in the follow-up of patients treated with testolactone. On the other hand, Werber Leschek et al. [28] confirmed the research findings of Laue et al. [25][26] in boys with FMPP, and further, they evaluated the effect of long-term antiandrogen (spironolactone), an aromatase inhibitor (testolactone or anastrozole), and gonadotropin-releasing hormone analog (GnRHa; deslorelin or depot leuprolide) on adult height in boys with FMPP. In their thirty-year study, testolactone was replaced by anastrozole after it was withdrawn from the market. The combined regimen of an antiandrogen, an aromatase inhibitor, and GnRHa substantially achieved the study goals of normalizing growth, development, and adult height [29].
Precocious puberty in girls with McCune–Albright syndrome (MAS) is usually due to ovarian estrogen secretion that is independent of pubertal hypothalamic pituitary activation. Isosexual precocity, due to increased ovarian estrogen secretion with recurrent formation of ovarian cysts, is the most endocrine abnormality in girls with McCune–Albright syndrome. The lack of an effect of LHRH agonists on the clinical and biochemical sings, suggests that sexual precocity is maintained by gonadotropin-independet, autonomous ovarian estrogen secretion. Because, treating with medroxyprogesterone and cyproterone acetate was not successful in suppressing all sings, Foster et al. [30] have treated a girl with McCune–Albright syndrome with testolactone. During testolactone therapy, menses ceased, bone age advancement and height velocity diminished, and plasma estradiol levels were suppressed. Serum gonadotrophin levels remained in the prepubertal range and testolactone was an effective therapy of precocious puberty in girls with McCune–Albright syndrome. Further, Hauffa et al. [31] have compared the short-term effects of testolactone, with those of cyproterone acetate, a combined therapy with medroxyprogesterone and spironolactone, and of surgery alone. In their conclusion, therapy with testolactone led to an absolute and relative decrease in height velocity, a normal rate of bone maturation, and to elevation of androstenedione plasma concentrations.
In their research of precocious puberty in girls with McCune–Albright syndrome, Feuillan et al. [32] concluded that testolactone decreased the levels of circulating estradiol and the ovarian volume, leading to a return to pretreatment levels after testolactone was stopped. Further, Feuillan et al. [33] applied testolactone therapy to two girls who did not have skin and bone lesions, but who developed precocious puberty independent of luteinizing hormone and were unresponsive to LHRH agonist therapy. One of these girls appeared to have benefited from testolactone. In their further studies of long-term use of testolactone therapy, they concluded that testolactone can be effective in the treatment of LHRH-independent precocious puberty in girls with McCune–Albright syndrome, but some patients exhibit an escape from the effects of the treatment after 1–3 years [34].
Gryngarten et al. [35] analyzed the cases of girls who were treated at the Department of Endocrinology of Hospital de Niños Ricardo Gutiérrez between 1974 and 2019. In their work they have applied medroxyprogesterone acetate, tamoxifen, testolactone, or letrozole in the treatment of these girls and have concluded that these drugs can contribute to the treatment of certain aspects of this illness, they can improve the quality of life.
Even though, MAS is predominantly observed in girls and is rarely reported in males, Papadopoulou et al. [36] report the case of a 9-year-old boy with gonadotropin-independent precocious puberty, café-au-lait spots, polyostotic fibrous dysplasia and growth hormone hypersecretion. After diagnosis, treatment with somatostatin long-acting analogs and testolactone was initiated. Testolactone was discontinued at the age of 13 and central puberty began shortly thereafter.
In her work, Zacharin [37] described the case of a boy with polyostotic fibrous dysplasia, acromegaly, and gonadotrophin-independent precocious puberty, which was treated with flutamide in combination with testolactone. An increase in hepatic enzymes and neutropaenia during the first 3 months was thought to be due to flutamide. Withdrawal of flutamide resulted in rapid normalization of the white cell count and reduction in liver enzymes. Testolactone was continued without further problems, which lead to a significant improvement in quality of life.

3. Gynecomastia

Gynecomastia is a condition of non-cancerous overdevelopment or enlargement of the breast tissue in men or boys. An imbalance of estrogen and testosterone in the body often leads to this condition, while in most cases, the tissue disappears spontaneously within a few years, but in some cases, hormone therapy was applied.
In their work Zachman et al. [38] described the use of testolactone in the treatment of boys with pubertal gynecomastia, where a significant increase in androstenedione levels and a significant decrease in mean breast diameter were observed. Similarly, Binder et al. [39] studied a family in which seven affected males over three generations had inherited prepubertal gynecomastia in an autosomal dominant manner. In their work, treatment was more effective with anastrozole than with testolactone and increased the initially reduced testes volume to normal size, promoted virilization, and normalized serum estrone and testosterone levels.
In the case report presented by Auchus and Lynch [40], testolactone was administered to men with unilateral gynecomastia, occurring after unilateral orchiectomy. Testolactone effectively treated this condition by raising the androgen-estrogen ratio without lowering absolute estradiol levels.
Kara et al. [41] studied a case of a boy with Peutz–Jeghers syndrome, bilateral gynecomastia, Sertoli cell tumor, and nephrocalcinosis. The aromatase inhibitor testolactone was administered in an attempt to prevent skeletal maturation. One-year treatment with testolactone reduced the breast base diameter, and there was no rapid advancement in his bone age.

4. Congenital Adrenal Hyperplasia (CAH)

Congenital adrenal hyperplasia (CAH) is an autosomal recessive condition with reduced glucocorticoid and mineralocorticoid biosynthesis, as a result of deletions or mutations of the cytochrome P450 21-hydroxylase gene, which leads to increased secretion of corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH), adrenal hyperplasia, and excessive production of cortisol and aldosterone [42][43].
Merke et al. hypothesized that by using antiandrogens in combination with an inhibitor of estrogen synthesis from androgens, the hydrocortisone dose could be reduced [43][44][45][46]. They have investigated the impact of the regimen of antiandrogen (flutamide), an aromatase inhibitor (testolactone), reduced hydrocortisone dose, and fludrocortisone compared to the effects of a control regimen of hydrocortisone and fludrocortisone in children with classic 21-hydroxylase deficiency. Additionally, they investigated the effect of flutamide alone, on cortisol clearance. Their findings demonstrate that the addition of flutamide and testolactone to the treatment regimen of hydrocortisone, significantly decreases cortisol clearance, but this effect seems to be due to flutamide [43].

5. Fertility and Sterility

In the 1980s, one of the research directions on fertility and sterility was based on the assumption that estradiol can indirectly affect spermatogenesis by preventing the Leydig cell from maximally producing testosterone in response to the luteinizing hormone. It was considered that, by decreasing estradiol formation, there might be an improvement in both sperm count and fertility in patients with infertility due to oligospermia. In this respect, Vigersky and Glass [47] investigated the influence of testolactone on spermatogenesis and the pituitary–testicular axis in men with idiopathic oligospermia. They concluded that after testolactone therapy there was a decrease in estrone and estradiol levels, followed by an increase in serum testosterone and androstenedione; further, there was an increase in the testosterone-estradiol ratio, and thus an improvement in spermatogenesis, with no effect on gonadotropin production in men.
In their works, Dony et al. [48][49] investigated whether sustained lowering of endogenous estrogen levels by chronic administration of testolactone might influence the anomalous Leydig cell response to luteinizing hormone-releasing hormone in patients with idiopathic oligospermia. They have concluded that testolactone lowered circulating estradiol, and thereby sex hormone binding globulin (SHBG), enhanced the secretion of follicle-stimulating hormone (in contrast to the investigation of Vigersky and Glass [47]), 17-hydroxyprogesterone and testosterone, but did not affect serum luteinizing hormone levels. Despite estradiol lowering, there was an accumulation of 17-hydroxyprogesterone over testosterone, suggesting 17,20-lyase inhibition. Although these investigations suggest that estrogens play a less dominant role in the origin of the late steroidogenic lesion than previously assumed, the suggestion also arises that testolactone per se, in addition to its antiestrogenic action, has an inhibiting effect on the 17,20-lyase, which may obscure the beneficial effect of reducing estradiol.
Maier and Hienert [50] investigated whether inhibition of testosterone catabolism by testolactone prevents the increase in the estradiol concentration during tamoxifen therapy and whether the ejaculate parameters or the incidence of gravidity can be further improved, compared to monotherapy with tamoxifen. Their results indicate that with additional administration of testolactone, the increase in estradiol levels on tamoxifen therapy is reduced, but not completely eliminated. With a combination therapy of tamoxifen and testolactone, no further improvement of the ejaculate parameters was seen and there is no advantage over monotherapy with testolactone.
Pavlovich et al. [51] identified an endocrinopathy in men with severe male factor infertility, characterized by a decreased serum testosterone-to-estradiol ratio. This ratio can be corrected when men were treated with testolactone, resulting in a significant improvement in semen parameters in oligospermic patients.
Dunaif et al. [52] have investigated the effects of testolactone on gonadotropin release and steroid metabolism in polycystic ovarian disease (PCOD). In their conclusions, testolactone was potent inhibitor of peripheral, but not ovarian aromatase in humans, and of hypothalamic aromatase in rats.
In order to obtain additional information concerning the site of action of testolactone on human testicular steroid production, Martikainen et al. [53] studied the effects of testolactone on a number of circulating steroid hormones and their sulfate conjugates and on serum luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin (PRL), and sex-hormone-binding globulin (SHBG) concentrations. Short-term testolactone treatment caused a partial inhibition of aromatization of androgens to estrogen in normal men and further inhibitory influence on the 17β-reduction of dehydroepiandrosterone and androstenendione. Increased serum concentrations of pregnenolone, 17-hydroxypregnenolone, and testosterone sulfates were also observed, but it remains unclear whether testolactone has a direct or possibly an estradiol-mediated effect on the steroid sulfates of testicular.
In order to assess the hormonal alterations that occur in the testolactone-therapy, Nagler et al. [54] used adult male rat model for studying the role of estrogens upon sperm production. They concluded that testolactone does not have an effect on the peripheral level of testosterone or estradiol and the data suggests that the blood production rate of estradiol in the male rat is not dependent upon the aromatization of peripheral testosterone.
Testolactone was used in order to examine whether there is feedback regulation of androgens/estrogens on prolactin secretion in the human male, while there is evidence that prolactin may be involved in testicular steroidogenesis. Gooren et al. [55] have measured basal and thyrotropin-releasing hormone (TRH)-stimulated prolactin levels in eugonadal and agonadal men after testolactone, spironolactone or dihydrotestosterone undecanoate treatment. They have concluded that in the human male, endogenous estrogens increased prolactin secretion, while exogenous/endogenous androgens decrease prolactin secretion.
In further investigation, by examining the influence of testosterone and testolactone on modulation of prolactin in normal women, Serafini et al. [56] have concluded that inhibition of aromatization by testolactone resulted in a significant increase in prolactin, which was similar to the increase which occurred with testosterone when testolactone was not administered.
In vivo studies demonstrated that treatment with aromatase inhibitors significantly alters the endogenous endocrine profile, especially estradiol, without concomitant alteration in rat ovarian histology at concentrations slightly above physiologic levels [57].
In their work, Marynick et al. [58] have confirmed that testolactone itself did not influence gonadotropin levels. They maintained serum testosterone and estradiol at constant physiological levels with infusion of testosterone, and then compared serum luteinising hormone (LH) and follicle stimulating hormone (FSH) levels before and during testolactone and estradiol administration, and no differences were found. Gooren et al. [59] have investigated the impact of estrogens in the feedback regulation of gonadotropin secretion. They have studied basal and luteinizing hormone-releasing hormone (LRH)-stimulated gonadotropin in a group of orchidectomized male-to-female transsexuals on estrogen treatment. Agonadal and eugonadal subjects have received ethinylestradiol or testolactone or tamoxifene and the levels of LH and FSH secretion were measured. The data in this research do not provide direct evidence that estrogen negative feedback occurs at the level of the hypothalamus or pituitary, and the authors have concluded that this is not an LRH-mediated phenomenon, but rather the result of a direct effect of estrogens at the level of the gonadotroph.
Smals et al. [60] investigated effect of lowering estradiol levels by testolactone on basal and gonadotropin stimulated Leydig cell function in men. After testolactone therapy, the observed a lowering of circulating estradiol levels, the enhancing of the secretion of FSH, 17-hydroxyprogesterone, and a lowering of the degree of testosterone without affecting on serum LH levels. In addition, there was greater accumulation of 17-hydroxyprogesterone than of testosterone, suggesting 17,20-lyase inhibition. Although Vigersky et al. [61] demonstrated that testolactone has antiandrogenic properties, androgen receptor blockade cannot account for the unexpected accumulation of 17-hydroxyprogesterone over testosterone; the authors concluded that testolactone exerts its 17,20-lyase blocking effect through another mechanism. While the aromatase-inhibiting action of testolactone has been attributed to its competition with testosterone and also androstenedione for microsomal aromatase cytochrome P450 [62], Smals et al. [60] have speculated that testolactone, as a pseudo/substrate, also competes for the binding sites of cytochrome P450 17,20-lyase, and leads to inhibition of both key enzymes. Thus relief of the 17,20-lyase block induced by estradiol lowering might be obscured by a concomitant action of testolactone.
Zumoff et al. [63] have applied testolactone to confirm their hypothesis that obese men have elevated serum estrogen levels and diminished levels of FSH and free and total testosterone, all in proportion to their degree of obesity. The decreases in testosterone and FSH constitute a state of hypogonadotropic hypogonadism (HHG), and authors have concluded that it results from feedback suppression of the pituitary by the elevated estrogen levels.
Epilepsy is a disease that can be controlled with drugs nowadays. However, taking drugs to control epilepsy often leads to androgen deficiency in men, which can affect reproduction, lead to sexual dysfunction, and even possibly exacerbate seizure frequency. The assumption is that antiepileptic drugs affect the conversion of testosterone to estradiol. These side effects could be controlled by testosterone therapy, which could have a moderate beneficial effect on reproductive and sexual functionality. While testosterone is thought to reduce the frequency of seizures, estradiol, on the other hand, has the opposite effect. For this reason, Herzog et al. [64] in their research compared the effect of testosterone therapy with the effect when testosterone was given in combination with the aromatase inhibitor testolactone. They concluded that combined therapy leads to the normalization of estradiol levels, and to greater improvement in sexual function than testosterone alone, and also to a reduction in seizure frequency, due to reduced estradiol levels.

6. Fibromatosis

Sauven [65] published a case report of musculo-aponeurotic fibromatosis treated by surgery and testolactone. This was the first case in which testolactone therapy was administered after complete excision of the lesion. She observed no side effects with this treatment and there was no increase in tissue in ten months.

7. Atherosclerotic Cardiovascular Disease

It is known that homocysteine can promote atherosclerosis, while levels are associated with increased risk for atherosclerotic cardiovascular diseases. While total homocysteine (tHcy) levels are known to be higher in men than in women, Zmuda et al. [66] hypothesized that sex hormones may influence their levels. With the goal to examine the influence of androgens on increasing levels of tHcy, Zmuda et al., in addition to testosterone, applied testolactone in order to examine the effects of the conversion of androgens into estrogens in patients. Subjects received testosterone enanthate, testolactone, or both drugs together in a crossover design, but testolactone did not significantly influence tHcy levels.

8. COVID-19

In April 2020, World Health Organization (WHO) declared Corona Virus Disease (COVID-19) as a global pandemic disease, and since then the search for an adequate drug has been current in scientific circles. It is known that COVID-19 was caused by the SARS-CoV-2 virus, from a group of pathogenic coronaviruses. Mujwar [67] has investigated the triple mutant strain of SARS-CoV-2, which was more virulent and pathogenic than its original strain, with a high mortality rate in the second wave of the coronavirus disease. In order to develop a potent inhibitor, molecular docking simulation-based virtual screening of a ligand library consisting of FDA-approved drugs, followed by molecular dynamics simulation-based validation of leads, was performed. In this investigation, testolactone was among the top ten drug molecules with good binding energy, but further investigations were not pursued.

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