Quinagolide hydrochloride - CAS 94424-50-7
Catalog number: 94424-50-7
Category: Inhibitor
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Dopamine Receptor
Quinagolide hydrochloride is a selective dopamine D2 receptor agonist, also is a prolactin inhibitor.
white solid powder
NORPROLAC, BRN 6074559; BRN6074559; BRN-6074559; CV205-502.
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Ferring Pharmaceuticals Inc.
1.In vivo inhibition followed by exogenous supplementation demonstrates galactopoietic effects of prolactin on mammary tissue and milk production in dairy cows.
Lollivier V;Lacasse P;Angulo Arizala J;Lamberton P;Wiart S;Portanguen J;Bruckmaier R;Boutinaud M J Dairy Sci. 2015 Dec;98(12):8775-87. doi: 10.3168/jds.2015-9853. Epub 2015 Sep 18.
It has been previously shown that the long-term inhibition of milking-induced prolactin (PRL) release by quinagolide (QN), a dopamine agonist, reduces milk yield in dairy cows. To further demonstrate that PRL is galactopoietic in cows, we performed a short-term experiment that used PRL injections to restore the release of PRL at milking in QN-treated cows. Nine Holstein cows were assigned to treatments during three 5-d periods in a 3×3 Latin square design: 1) QN: twice-daily i.m. injections of 1mg of QN; 2) QN-PRL: twice-daily i.m. injections of 1mg of QN and twice-daily (at milking time) i.v. injections of PRL (2µg/kg body weight); and 3) control: twice-daily injections of the vehicles. Mammary epithelial cells (MEC) were purified from milk so that their viability could be assessed, and mammary biopsies were harvested for immunohistological analyses of cell proliferation using PCNA and STAT5 staining. In both milk-purified MEC and mammary tissue, the mRNA levels of milk proteins and BAX were determined using real-time reverse-transcription PCR. Daily QN injections reduced milking-induced PRL release. The area under the PRL curve was similar in the control and PRL injection treatments, but the shape was different.
2.Ca(2+)-dependent protein kinase C isoforms in rat pituitary hyperplasia: effect of in vivo treatment with quinagolide.
Lévy L;Alvaro V;Dubray C;Joubert D Eur J Pharmacol. 1994 Aug 16;268(3):327-34.
Ca(2+)-dependent protein kinase C (PKC) activity, diacylglycerol levels and PKC alpha, beta I, beta II and gamma expression were analyzed in the pituitary of female rats treated with estradiol alone (2 months) or in combination with quinagolide in the second month. Polymerase chain reaction (PCR) and Western blot analysis revealed the presence of PKC alpha, beta I and beta II isoenzymes in the rat pituitary gland but not of PKC gamma isoenzymes. Increases in pituitary weight and plasma prolactin levels induced by estradiol were associated with an increase in diacylglycerol pituitary content (1.55 +/- 0.06 versus 1.12 +/- 0.17 nmol diacylglycerol/mg protein in controls, P < 0.01). Cotreatment with quinagolide reversed these effects. Changes in PKC activity were accompanied by parallel changes in PKC alpha and beta I expressions. Estradiol treatment increased the expression of these isoforms whereas cotreatment with quinagolide antagonized these effects. PKC beta II expression was not affected. In conclusion, Ca(2+)-dependent PKC activity and protein expression are increased in hyperplastic pituitary cells, suggesting the involvement of this class of PKCs in the rat pituitary cell proliferation and/or hormonal secretion.
3.Rapid re-enlargement of a macroprolactinoma after initial shrinkage in a young woman treated with bromocriptine.
Adler I;Barsi P;Czirják S;Varga I;Gergics P;Jakab C;Rácz K Gynecol Endocrinol. 2005 Jun;20(6):317-21.
We report the case of a macroprolactinoma in a 32-year-old woman, who presented with secondary amenorrhea, galactorrhea, increased plasma prolactin level (3259 ng/ml), headache and bi-temporal visual field defect. Magnetic resonance imaging showed a large pituitary tumor. The patient responded well to bromocriptine (7.5 mg/day) with improvement of clinical symptoms and normalization of plasma prolactin within a few weeks. After 4 months of treatment, tumor size was also reduced markedly. During continued treatment at the same dose of bromocriptine the plasma prolactin level remained normal, but after 8 months of treatment the patient suddenly complained of worsening of her visual fields, and magnetic resonance imaging indicated re-enlargement of the tumor. Bromocriptine was discontinued and transsphenoidal pituitary surgery was performed. After surgery the visual field defect improved, but postoperative plasma prolactin level (1104 ng/ml) and magnetic resonance imaging indicated a residual tumor. Postoperative treatment with quinagolide (0.15 mg/day) resulted in disappearance of all clinical symptoms, normalization of prolactin level and a reduction in size of the residual tumor. This case demonstrates that a dissociation of the inhibitory effect of bromocriptine on tumor size and prolactin level may rarely develop during the course of drug treatment in a patient with macroprolactinoma.
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CAS 94424-50-7 Quinagolide hydrochloride

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