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PubMed1995

The effect of medrogestone on plasma lipids and lipoproteins in postmenopausal women using conjugated estrogens: an open randomized comparative study.

OBJECTIVE: To test the hypothesis that the progestogen medrogestone has no effect on changes in lipoprotein metabolism evoked by continuous estrogen replacement therapy, paying special attention to high-density lipoproteins (HDL). DESIGN: Open multicenter randomized comparative trial. PATIENTS: Postmenopausal hysterectomized women aged 49 to 64 years. INTERVENTION: Continuous oral treatment with 0.625 mg daily of conjugated estrogens (CE) alone (n = 55) or CE plus 5 mg of the progestogen medrogestone orally during the last 12 days of each 28-day cycle (n = 59). MAIN OUTCOME MEASURES: At baseline and at cycles 3, 6, and 13 we measured the plasma levels of apolipoprotein (Apo) A1, cholesterol in total HDL and in its subfractions HDL2 and HDL3, using density gradient ultracentrifugation. RESULTS: High-density lipoprotein cholesterol increased from baseline at all assessments in both treatment groups, being significantly greater in the CE group (+15% at cycle 13) than in the CE and medrogestone group (+8%). However, HDL2-cholesterol increased in both treatment groups, but with no significant difference between the two groups. High-density lipoprotein 3 cholesterol increased only in the CE group (+7% at cycle 13); there was no significant change in HDL3-cholesterol in the CE and medrogestone group. Low-density lipoprotein (LDL) cholesterol decreased from baseline at all assessments in both treatment groups (-6% and -9%, respectively, at cycle 13). The change in very low-density (VLDL) lipoprotein cholesterol was not significant in either of the two groups. Medrogestone had no significant effects on the estrogen-induced increases in apo A-1 and triglycerides nor on the decreases in ApoB and LDL-cholesterol. Neither hormone significantly affected VLDL-cholesterol or Lp(a) levels. CONCLUSION: Medrogestone did not eliminate the increase in plasma HDL levels evoked by CE.

Apolipoprotein A-I↗
PubMed1975

Differences in the mechanism of action of medrogestone and cyproterone acetate.

In the intact adult rat, medrogestone was found to be effective in causing the involution of the prostate and seminal vesicle. Medrogestone, however, does not function through an antiandrogenic action. In the castrate animal medrogestone was unable to block the stimulating action of exogenous testosterone on the sex accessory organs as shown by effects on tissue weight and DNA synthesis. In addition, medrogestone was unable to block the uptake of labeled androgen into prostatic nuclei. The effectiveness of medrogestone on sex accessory tissue may be accounted for by its ability to lower plasma testosterone levels. This is achieved by inhibiting testosterone biosynthesis. The action of medrogestone was compared to that of cyproterone acetate and it was concluded that these drugs inhibit prostatic growth through two different mechanisms.

Androgens↗
PubMed1996

Sequential addition of low dose of medrogestone or medroxyprogesterone acetate to transdermal estradiol: a pilot study on their influence on the endometrium.

We evaluated bleeding pattern and endometrium following the administration of two of the most common types of progestogens used in hormone replacement therapy, medroxyprogesterone acetate (MPA) and medrogestone acetate. Twenty eight patients in spontaneous menopause were randomly allocated to two groups. Group 1 (n = 14) received 5 mg/day of of MPA and group 2 (n = 14) received 5 mg/day of medrogestone: both the progestogens were sequentially added for the last 12 days of a 21-day period of transdermal estradiol administration (50 micrograms per day). A 7-day treatment-free period completed the cycle. The study treatments were administered for 6 cycles. The endomtria were checked for their thickness by transvaginal ultrasound before starting treatment and at 6th treatment cycle (days 6-10 of the estrogen-only phase and during the period between days 8 and 12 of the progestogen addition). Endometrial biopsies were performed before starting treatment only in the patients with a positive progesterone challenge test and in all the patients at the end of the study during the addition of the progestogen. The bleeding pattern was closely monitored. MPA is accompanied by a thick endometrium with full secretory transformation in all cases. On the contrary, the same dose of medrogestone induced a consistent decrease of estrogen primed endometrium with only 4 cases of full secretory transformation. Four medrogestone-treated patients dropped out due to unscheduled bleeding. A low dose of medrogestone added to transdermal estradiol induced incomplete transformation of endometrium and oligo-amenorrhea more frequently than MPA, but it increased the chances of irregular bleeding. MPA fully transformed the endometrium: periods were thus heavier but regular. None of the patients in either group had endometrial hyperplasia.

Administration, Cutaneous↗
PubMedDate not supplied

Control of sulfatase and sulfotransferase activities by medrogestone in the hormone-dependent MCF-7 and T-47D human breast cancer cell lines.

In the present study, we explored the effect of the progestin medrogestone on the sulfatase and sulfotransferase activities in the hormone-dependent MCF-7 and T-47D human breast cancer cell lines. After 24 h incubation at 37 degrees C of physiological concentrations of estrone sulfate ([3H]-E1S: 5x10(-9) mol/l), it was observed that this estrogen was converted in a great proportion to E2 in both cell lines. Medrogestone significantly inhibits this transformation, at all the concentrations tested (5x10(-8) to 5x10(-5) mol/l), in both cell lines. The IC50 values were 1.93 micromol/l and 0.21 micromol/l in MCF-7 and T-47D cells, respectively. In another series of studies, after 24 h incubation at 37 degrees C of physiological concentrations of estrone ([3H]-E1: 5x10(-9) mol/l), the sulfotransferase activity was detectable in both cell lines. Estrogen sulfates (ES) are found exclusively in the culture medium, which suggests that as soon as they are formed they are excreted into the medium. Medrogestone has a biphasic effect on sulfotransferase activity in both cell lines. At low doses: 5x10(-8) and 5x10(-7) mol/l, this compound stimulates the enzyme by +73.5 and 52.7%, respectively, in MCF-7, and by 84.5 and 62.6% in T-47D cells. At high concentrations: 5x10(-6) and 5x10(-5) mol/l, medrogestone has no effect on MCF-7 cells, but inhibits the sulfotransferase activity in T-47D cells by -31.4% at 5x10(-5) mol/l. In conclusion, the inhibitory effect provoked by medrogestone on the enzyme involved in the biosynthesis of E2 (sulfatase pathway) in estrogen-dependent breast cancer, as well as the stimulatory effect on the formation of the inactive ES, support a probable anti-proliferative effect of this progestin in breast tissue. Clinical applications of these findings can open new therapeutic possibilities for this disease.

Antineoplastic Agents, Hormonal↗
PubMed1999

Add-back medrogestone does not prevent bone loss in premenopausal women treated with goserelin.

To investigate the effect of medrogestone on bone mineral density (BMD) and bone turnover under conditions of estrogen withdrawal, premenopausal women with endometriosis were treated with goserelin (Zoladex), combined with either placebo (group A, n = 12) or 10 mg medrogestone (Prothil, group B, n = 11) for six months, and followed for an additional six months. Lumbar spine BMD was measured at 0 and 6 month. Markers of bone turnover were serum bone alkaline phosphatase (sBAP) and osteocalcin (sOC) by ELISA, and urinary total pyridinoline (uPYD) and deoxypyridinoline crosslinks (uDPD) by HPLC. Patients in both groups had a similar and significant decrease in BMD after 6 months (4%, p < 0.01). The time course of changes in bone turnover, in contrast, was different in both groups. In group A, crosslink excretion increased from one month onwards, while no changes were seen in group B. In group A, sBAP levels rose during treatment, while in group B, this rise was delayed until treatment was terminated. Additionally, group B showed an initial suppression of sBAP and sOC. In both groups, sOC increased after treatment was discontinued. Medrogestone at 10 mg/d does not prevent lumbar bone loss in premenopausal women under estrogen deprivation. In the medrogestone add back group, the changes in bone turnover are compatible with low turnover bone loss,as ooposed to a state of high turnover seen in the unopposed goserelin group. This effect may be due to glucocorticoid receptor mediated actions of medrogestone on bone.

Adult↗
PubMed2000

[Effect of combined conjugated estrogen-medrogestone replacement therapy on lipid profiles, climacteric symptoms and the endometrium].

OBJECTIVE: To assess the effects of continuous administration of conjugated estrogen combined with sequential administration of medrogestone on lipid profiles, climateric symptoms and endometrial tolerance. METHODS: This multicenter open study was conducted for one year to assess the effects of a hormone replacement therapy (HRT) regimen using Premarin (0.625 mg/day 28d/28) combined with medrogestone 5mg for 12 days (d17-d28 of each 28-day cycle) on lipid profiles, climateric symptoms and cycle control in 228 post menopausal women with an intact uterus. The subjects were recruited in 23 centers in 7 countries in Europe and Asia. Serum lipid/lipoprotein levels were determined at baseline and at cycles 3, 6, 13; endometrium biopsies were performed at screening then at cycle 13. Climateric symptoms and bleeding patterns were recorded by the patients from daily diaries cards collected at baseline and at visits during cycle 3, 6, 9, and 13. RESULTS: By cycle 3, the conjugated estrogen-medrogestone combination induced significant modifications of the lipid profile which were judged favorable. These modifications were maintained throughout treatment. All the baseline values were within normal limits. Mean variations compared with baseline values (expressed in mmol/l) after cycles 3, 6, and 13 were -0.46, -0.54, and -0.46 for total cholesterol (p<0.05), + 0.053, + 0.057, and + 0.078 for HDL-cholesterol (p<0.05) and -0.556, -0. 542, and -0.493 for LDL-cholesterol (p<0.001) respectively. VLDL-cholesterol levels were unchanged. Triglycerides increased significantly though moderately: + 0.12, + 0.15, and + 0.15 mmol/l at cycles 3, 6, and 13 respectively. Endometrial biopsies obtained at cycle 13 (n=195) did not reveal any endometrial hyperplasia. Withdrowal bleeding was predictable for a 6 to 7.4 day interval. The incidence of irregular bleeding varied from 7 to 33% and decreased progressively over the 13-cycle treatment. The incidence of amenorrhea increased from 14 to 52% over the 12 months studied. Finally, at each cycle, menopausal symptoms (mean number of hot flushes/day and Küpperman score) were significantly improved compared with the baseline. As expected, modifications were more pronounced after cycle 1, but improvements were maintained throughout the study. CONCLUSION: Continuous administration of Premarin in combination with sequential administration of medrogestone was found to be an effective treatment for menopausal symptoms. It was associated with favorable modifications of the lipid profile and was safe for the endometrium.

Aged↗
PubMed1975

Medrogestone: a prospective study in the pharmaceutical management of benign prostatic hyperplasia.

Medrogestone is a progestational agent that may reduce outflow obstruction secondary to benign prostatic hyperplasia. Five of 8 patients taking 15 mg. oral medrogestone twice daily and 5 of 7 patients taking 7.5 mg. oral medrogestone twice daily experienced an increase in mean urine flow (averaging 55.8 and 30.1 per cent, respectively), while no change was noted in 4 untreated patients. Five of the 8 patients taking 15 mg. and 6 of the 7 patients taking 7.5 mg. experienced an increase in peak urine flow (averaging 60 and 37.6 per cent, respectively), while 2 of the 4 controls had an improvement of only 12.2 per cent. Repetitive residual urines and digital examination were inaccurate to assay sequential changes in prostatic size. Certain side effects, such as hypertension, abnormal glucose tolerance and impotence, were encountered in isolated patients but in no instance was the side effect hazardous to the health of the test subject and in each instance it could be reversed by withdrawal of the medication.

Clinical Trials as Topic↗
PubMed1999

Effect of Medrogestone on 17beta-hydroxysteroid dehydrogenase activity in the hormone-dependent MCF-7 and T-47D human breast cancer cell lines.

Estradiol (E2) is one of the most important hormones supporting the growth and evolution of breast cancer. Consequently, to block this hormone before it enters the cancer cell, or in the cell itself, has been one of the main targets in recent years. In the present study we explored the effect of Medrogestone (Prothil) on 17beta-hydroxysteroid dehydrogenase (17beta-HSD) activities of the hormone-dependent MCF-7 and T-47D human breast cancer cell lines. Using physiological doses of estrone ([3H]-E1: 5 x 10(-9) mol/l) this estrogen is converted in a great proportion to E2 in both cell lines. After 24 h of the cell culture, Medrogestone significantly inhibits this transformation in a dose-dependent manner by 39% and 80% at 5 x 10(-8) M and 5 x 10(-5) M, respectively in T-47D cells; the effect is less intense in MCF-7 cells: 25% and 55% respectively. The IC50 values are 0.45 micromol/l in T-47D and 17.36 micromol/l in MCF-7 cells. It is concluded that the inhibition provoked by Medrogestone on the reductive 17beta-HSD activity involved in the local biosynthesis of the biologically active estrogen estradiol, may constitute a new therapeutic approach for the treatment of breast cancer.

17-Hydroxysteroid Dehydrogenases↗
PubMed1990

Effects of conjugated equine oestrogens with and without the addition of cyclical medrogestone on hot flushes, liver function, blood pressure and endocrinological indices.

Despite widespread clinical use of conjugated oestrogens, there is a paucity of reported studies concerning the effect of such therapy in sequential combination with the progestin, medrogestone (Colpro; Akromed). In a double-blind study, 22 oestrogen-deficient women who had undergone hysterectomy (mean age 52,8 years) were treated initially for 6 cycles with either conjugated equine oestrogens 0.625 mg (CEE) for 21 days plus a placebo during the last 10 days of each cycle or the same oestrogen regimen with 10 days of medrogestone 5 mg/d. Thereafter the treatments were crossed over for a further 6 cycles. CEE monotherapy resulted in significantly decreased levels of follicle-stimulating hormone (FSH), luteinising hormone (LH), prolactin (PRL) (P less than 0,001) and gamma-glutamyl transferase (P less than 0,01) with an increase in 17 beta-oestradiol (P less than 0,001). Medrogestone had a synergistic effect on the lowering of FSH, LH and PRL. No treatment modality caused any significant changes in blood pressure, fasting glucose value or vaginal cellular percentages. The decrease in hot flush scores, already manifest at the end of the first cycle, were sustained throughout (P less than 0,001).

Blood Pressure↗
PubMed1989

Serum lipoprotein effects of conjugated estrogen and a sequential conjugated estrogen-medrogestone regimen in hysterectomized postmenopausal women.

The progestogen chosen for addition to estrogen replacement is important because some progestins adversely influence the effects of oral estrogens on lipid metabolism. In this double-blind study, 22 estrogen-deficient hysterectomized women were treated initially for six cycles with either 0.625 mg conjugated equine estrogens for 21 days plus a placebo during the last 10 days of each cycle or the same estrogen regimen with 10 days of 5 mg medrogestone per day. Thereafter, the treatments were crossed over for a further six cycles. Levels of lipids, lipoproteins, and apolipoproteins were determined at baseline and the last day of sixth and twelfth treatment cycles. Conjugated equine estrogen monotherapy resulted is significantly increased levels of high-density lipoprotein cholesterol (p less than 0.01); percent high-density lipoprotein cholesterol (p less than 0.001), and high-density lipoprotein2-cholesterol (p less than 0.001), with significantly decreased total cholesterol (p less than 0.01), low density lipoprotein cholesterol, and atherogenic index (p less than 0.001). Medrogestone caused no attenuation of any of these clinically important lipoprotein changes. Therefore from the lipoprotein aspect medrogesterone is a desirable progestogen.

Double-Blind Method↗
PubMed1994

Effect of conjugated estrogens with and without medrogestone: a prospective study.

OBJECTIVE: To study the possible changes in serum lipids and lipoproteins during hormone replacement therapy with special emphasis on the possible effects brought about by the progestogen. DESIGN: Open-label randomized prospective comparative study. SETTING: Gynecological outpatient department of an university hospital. PATIENTS: Thirty-three healthy hysterectomized postmenopausal women. INTERVENTIONS: Continuous oral supplementation with conjugated estrogens, 0.625 mg daily, was administered either alone (group I; N = 18) or in combination with cyclic medrogestone, 5 mg daily during the last 12 days of each 28 days treatment cycle (group II; N = 15). MAIN OUTCOME MEASURE: Changes in serum lipids, lipoproteins and apolipoproteins after three, six and 13 treatment cycles. RESULTS: After 1 year of treatment significant increases were observed in mean high-density lipoprotein (HDL) cholesterol, its subfractions, and apolipoprotein A-I in group I and II: HDL cholesterol: +25.2% and +12.1%, respectively; HDL2 cholesterol: +47.4% and +23.5%, respectively; HDL3 cholesterol: +18.1% and +11.2%, respectively; apolipoprotein A-I: +23.0 and +14.8%, respectively. Comparing the two study groups no significant differences were found in lipid changes during the study period, except for HDL2 cholesterol. CONCLUSION: Supplementation with conjugated estrogens, with and without medrogestone, and given for a longer period, demonstrated a beneficial influence on serum lipoproteins with almost no differences between the two treatment regimens.

Administration, Oral↗
PubMed1998

Determination of medrogestone in plasma by high-performance liquid chromatography.

Interference with the UV absorbance of medrogestone by endogenous steroids in plasma was prevented by reacting plasma with oxalyl chloride. The reduction of interference was effective when oxalyl chloride was in the range 10-50 microl/ml plasma. Reaction of oxalyl chloride with plasma for 10 min could reduce interference approximately 5.5-fold, and there was no significant reduction after 30 min. The limit of quantitative concentration for medrogestone in HPLC was 1 ng/ml. The standard curves were linear with the correlation coefficient greater than 0.999 in the range of 1-30 ng/ml. The coefficients of variation of both intra- and inter-day mean values were <12% and <10% of the actual values, respectively. The developed method for plasma sample preparation and the evaluated HPLC condition were further applied to an in vivo pharmacokinetic study.

Adult↗
PubMed1982

Medrogestone and an LHRH analogue as potential combination therapy for hormone-dependent cancers.

Treatment (5 mg/kg s.c. for 1 to 4 weeks) of adult male rats with medrogestone (Colprone), a compound with progestational and antiandrogenic properties, induced significant atrophy of the ventral prostate without affecting testicular weight, testicular LH/hCG receptor levels or plasma testosterone. The potent LHRH agonist (D-Ala6, des-Gly-NH210) LHRH ethylamide at 500 ng s.c. for 2-4 weeks suppressed the testicular weight, testicular LH/hCG receptor levels, plasma testosterone levels, and caused atrophy of the androgen-dependent seminal vesicles and ventral prostate. The combination 4 week-treatment of medrogestone and LHRH agonist led to the most significant decrease of prostatic weight. The potential usefulness of this combination therapy in hormone-dependent cancers is discussed.

Animals↗
PubMed1979

Medrogestone: analysis in serum by high-pressure liquid chromatography.

A method for the determination of 6,17-dimethylpregna-4,6-diene-3,20-dione (medrogestone) in serum is described using high-pressure liquid chromatography with UV detection. Interfering substances in human or dog serum blanks were removed selectively by reaction with oxalyl chloride followed by an aqueous alkaline borate "wash" of the extract. The method is specific for medrogestone and, based on 5 ml serum, has a limit of detection of 2 ng/ml.

Animals↗
PubMed1985

Effects of medrogestone and conjugated oestrogens on serum lipid and lipoprotein concentrations.

Twenty patients, aged 30-60 yr, who had undergone bilateral ovariectomy, were treated orally with 5 mg medrogestone (6,17-dimethylpregna-4,6-diene-3,20-dione) and 1.25 mg conjugated oestrogens per day, according to a constant dosage pattern during the cycle (22 + 6 days). The lipids and lipoproteins were determined twice before the start of therapy and 3, 6 and 12 mth thereafter. The lipids were quantified enzymatically and the lipoproteins by quantitative lipoprotein electrophoresis. Whilst cholesterol and triglyceride concentrations showed no detectable change, a slight but significant increase was seen in the high-density alphalipoprotein (HDL) cholesterol concentrations. The low-density beta-lipoprotein (LDL) cholesterol level showed a moderate fall. There was a resultant reduction in the beta/alpha-lipoprotein ratio. Accordingly, the apoprotein A1 concentrations were found to be elevated, while apoprotein B tended to fall to lower levels during therapy. When these changes are measured by the lipid metabolism risk criterion for the occurrence of coronary heart disease applicable to post-menopausal patients, the effects of the above-mentioned combination may be regarded as entirely favourable.

Adult↗
PubMed2002

Bleeding patterns in peri and postmenopausal women taking a continuous combined regimen of estradiol with norethisterone acetate or a conventional sequential regimen of conjugated equine estrogens with medrogestone.

OBJECTIVES: The aim of this study was to compare the incidence of women presenting irregular bleeding episodes following 9 months of treatment with a low dose continuous combined hormone replacement therapy consisting of estradiol (E(2)) and norethisterone acetate (NETA) versus a sequential hormone replacement therapy consisting of conjugated equine estrogens (CEE) and medrogestone (MG). Secondary aims were to establish the relationship between menopausal age and the occurrence of irregular bleeding for both therapies and to assess the efficacy of both therapies in alleviating menopausal symptoms. METHODS: This was a stratified and randomised, open label study conducted with late peri and postmenopausal women at 35 sites in Austria and Germany. A total of 446 women were randomly allocated into two cohorts based on time since last bleeding and then stratified to either a low dose continuous combined therapy consisting of 1 mg E(2) and 0.5 mg NETA for 28 days or a sequential therapy consisting of 0.625 mg CEE for 28 days and 5 mg MG for the final 14 days. Bleeding and menopausal complaints were continuously assessed. Treatments were administered for 9 lunar months. RESULTS: The incidence rate of women presenting irregular bleeding episodes including spotting during cycle 9 was 12.2% with 1mgE(2)/0.5mgNETA and 25.8% with 0.625mgCEE/5mgMG (P = 0.0014). In the group of postmenopausal women (time since last bleeding > or = 12 months) the incidence of irregular bleeding during cycle 9 was 11.0% for 1mgE(2)/0.5mgNETA and 25.0% for 0.625mgCEE/5mgMG). In the group of late perimenopausal women (time since last bleeding 6-11 months) the incidence of irregular bleeding was similar for both treatments at cycle 3, but markedly less in patients with 1mgE(2)/0.5mgNETA at cycle 6 and 9, being significantly different compared to patients with 0.625mgCEE/5mgMG at cycle 6 (P < 0.05). The cumulative rate of amenorrhea (no bleeding or spotting) achieved with 1mgE(2)/0.5mgNETA was 89% for the postmenopausal women and 83.7% for the late perimenopausal women. Both treatments relieved menopausal complaints equally effective. CONCLUSIONS: Regarding the occurrence of irregular bleeding, the low dose continuous combined therapy was superior to the sequential therapy (0.625mgCEE/5mgMG). The low dose continuous combined E(2)/NETA regimen is also suitable for late perimenopausal women since more than 80% of the women had no bleeding or spotting after 9 months of treatment.

Adult↗
PubMed1996

The effects of estradiol valerate plus medroxyprogesterone acetate and conjugated estrogens plus medrogestone on climacteric symptoms and metabolic variables in perimenopausal women.

BACKGROUND: Two sequential hormone replacement regimens, containing either estradiol valerate plus medroxyprogesterone acetate (E2V/MPA) or conjugated estrogens plus medrogestone (CE/MED), were compared with respect to effects on climacteric symptoms, lipid metabolism, and hemostasis. METHODS: In an open, multicenter study, 51 perimenopausal women were randomized to E2V/MPA and 50 to CE/MED. Assessment of climacteric complaints was performed at baseline and at months 1, 3, and 6. The effects on lipid and hemostatic variables were measured at baseline and at month 6. Quantitative data were analyzed using analysis of variance, the paired t-test or the chi2 Mantel-Hanszel test, where appropriate. RESILTS: Efficacy regarding treatment of climacteric symptoms was with E2V/MPA as good as with CE/MED, with a statistically significant reduction of most symptoms in both groups. After 6 months, total cholesterol and triglycerides had remained unchanged in both groups. High-density lipoprotein cholesterol showed no significant change with E2V/MPA, whereas an increase was noted in the CE/MED group (p<0.05). Low-density lipoprotein cholesterol was decreased with E2V/MPA (p<0.01) and was unchanged in the CE/MED group. Hemostatic parameters showed no significant changes after 6 months, with the exception of a decreased prothrombin time with E2V/MPA (p<0.05). Acceptability was excellent, expressed by the low incidence of treatment-related drop-outs in both groups. CONCLUSIONS: E2V/MPA is a one tablet per day sequential HRT regimen, which is as effective and acceptable as hormone replacement therapy with CE/MED regarding treatment of climacteric symptoms. Neither preparation had negative effects on lipid metabolism and hemostatic variables.

Adult↗
PubMed1981

Effect of medrogestone on conversions of pregnenolone and 17 alpha-hydroxypregnenolone in rat testis.

Medrogestone, viz., 6,17-dimethylpregn-4,6-diene,3,20-dione (Colprone), a synthetic compound with progestational and antiandrogenic properties, was studied for its effects on the metabolism of pregnenolone and 17 alpha-hydroxypregnenolone by a 10,000 g supernatant fraction of testicular homogenates. This compound inhibited the conversion of pregnenolone to progesterone (91%), 17 alpha-hydroxyprogesterone (83%), delta 4-androstenedione (43%), and testosterone (30%) and the conversion of 17 alpha-hydroxypregnenolone to 17 alpha-hydroxyprogesterone (84%), delta 4-androstenedione (56%), and testosterone (38%).

17-alpha-Hydroxypregnenolone↗