The Mechanism of Antiandrogenic Action of Chlormadinone Acetate

Kurosawa, Isao; Yamanaka, Hidetoshi; Koya, Atsushi; Imai, Kyoichi; Kosaku, Nozomu; Shida, Keizo

doi:10.5980/jpnjurol1928.68.6_537

Cited by 23 publications

(25 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…3, Table 1). Possible participation of the central nervous system in the secretion of pituitary gonadotropin and testicular androgen is usually regarded as the main cause of a decrease in testis weight and the serum androgen level [13]. It is, however, reasonable to suppose that the inhibitory effects of the two compounds are mainly attributable to their direct action on the prostate and testis rather than due to a decrease in the pituitary gonadotropin and testicular androgen secretion.…”

Section: Discussionmentioning

confidence: 96%

An Inhibitory Effect of TZP-4238 on the Growth of Androgen-Sensitive Rat Prostatic Tumor (Dunning R3327).

1993

View full text Add to dashboard Cite

Abstract. An inhibitory effect of TZP-4238, a newly synthesized antiandrogen, on the growth of Dunning R3327 rat prostatic tumor was studied and compared with that of chlormadinone acetate (CMA). TZP-4238 markedly suppressed the growth of R3327 tumor. The inhibitory effect of TZP-4238 on the tumor was more potent than that on the prostate. While the inhibitory effect of TZP-4238 on the weight of the ventral prostate was about 6 times as great as that of CMA, the suppressive effect of TZP-4238 on tumor weight was about 40 times as great as that of CMA. Serum levels of testosterone and dihydrotestosterone showed no obvious changes after the administration of either TZP-4238 or CMA. The inhibitory effect of TZP-4238 on the growth of R3327 tumor indicated the application of the compound to human prostatic cancer.

show abstract

Section: Discussionmentioning

confidence: 96%

An Inhibitory Effect of TZP-4238 on the Growth of Androgen-Sensitive Rat Prostatic Tumor (Dunning R3327).

1993

View full text Add to dashboard Cite

show abstract

“…In addition, loss of secretory and metabolic activities were evident. It is a well documented fact that CMA inhibits the uptake of testosterone in the prostate and is selectively incorporated into prostate cells, resulting in inhibiting testosterone binding to the cytosol 5 alpha-DHTreceptor [12,24,25]. In fact, the intensity of the immunostaining of nuclear AR in both epithelia and fibro-muscular stromal cells is dose-dependently weakened by treatment with CMA (Table 2).…”

Section: Atrophic Effect Of Antiandrogenmentioning

confidence: 93%

“…Chlormadinone acetate (CMA) is a steroidal antiandrogen that is widely used in the medical management of human BPH or prostatic carcinoma [9,12]. Histologically, CMA produced marked atrophy of the glandular epithelium (Tables 1, 2).…”

Section: Atrophic Effect Of Antiandrogenmentioning

confidence: 99%

Immunohistochemistry of the Canine Prostate.

Murakoshi

Ikeda

Tagawa

2001

Acta Histochem. Cytochem.

View full text Add to dashboard Cite

“…The atrophic effect of CMA on the human prostatic hyperplasia has been reported by several authors [8,11]. The antiandrogenic mechanisms of CMA has been evaluated biochemically and immunohistochemically, such as androgen receptor content, and steroid 5a-reductase type II activity in the prostate [11,[19][20][21][22].…”

Section: Introductionmentioning

confidence: 99%

“…Chlormadinone acetate (CMA) is a steroidal antiandrogen that is widely used in the medical management of human BPH or prostatic carcinoma [8,11]. The atrophic effect of CMA on the human prostatic hyperplasia has been reported by several authors [8,11].…”

Section: Introductionmentioning

confidence: 99%

Chlormadinone Acetate (CMA) Induces Apoptosis on Canine Spontaneous Benign Prostatic Hyperplasia (BPH).

Murakoshi

Ikeda

Fukui

et al. 2001

Acta Histochem. Cytochem.

View full text Add to dashboard Cite

The effect of a synthetic steroidal antiandrogen, chlormadinone acetate (CMA), on spontaneous benign prostatic hyperplasia (BPH) in dogs was investigated. Male beagle dogs (5-8 years old) were divided into four experimental groups. Group 1 consisted of untreated controls. Groups 2 to 4 received CMA 0.03, 0.1, and 0.3 mg/kg/day, p.o., respectively, for 6 months. In group 1, glandular hyperplasia of the prostate was clearly detected. In groups 2 to 4, CMA produced marked atrophy of the glandular epithelium. The interacinar fibro-muscular stroma was prominent. To evaluate the frequency of apoptosis, we counted the positive cells stained by the nick end labeling method. In group 1, the apoptotic index was 0.76H0.03%. In groups 2 to 4, apoptotic indices were 15.41H1.26%, 2.63H0.98% and 1.45H0.85%, respectively. Apoptotic cell death was mainly observed in the glandular epithelial cells. Based on our data, regression of BPH after treatment with CMA may be apoptotic cell death.

show abstract

The Mechanism of Antiandrogenic Action of Chlormadinone Acetate

Cited by 23 publications

References 0 publications

An Inhibitory Effect of TZP-4238 on the Growth of Androgen-Sensitive Rat Prostatic Tumor (Dunning R3327).

An Inhibitory Effect of TZP-4238 on the Growth of Androgen-Sensitive Rat Prostatic Tumor (Dunning R3327).

Immunohistochemistry of the Canine Prostate.

Chlormadinone Acetate (CMA) Induces Apoptosis on Canine Spontaneous Benign Prostatic Hyperplasia (BPH).

Contact Info

Product

Resources

About