Ulipristal Acetate 126784-99-4 large in supply CAS NO.126784-99-4

HRP 2000 Basic information

Product Name: HRP 2000
Synonyms: HRP 2000;(11b)-17-(Acetyloxy)-11-[4-(dimethylamino)phenyl]-19-norpregna-4,9-diene-3,20-dione;CBD 2914;VA 2914;Ulipristal;Ulipristal acetate;Ulipristal acetate/CDB2914;17α-Acetoxy-11β-(4-dimethylaminophenyl)-19-norpregna-4,9-dien-3,20-dione
CAS: 126784-99-4
MF: C28H35NO3
MW: 433.5824
EINECS: 
Product Categories: API;Aromatics;Intermediates & Fine Chemicals;Isotope Labelled Compounds;Pharmaceuticals;Steroids;Final material
Mol File: 126784-99-4.mol

Ulipristal Acetate Chemical Properties
Melting point  183-185 ºC
density  1.19

Description Ulipristal acetate (UPA) is a selective progesterone receptor modulator. Attributing to its higher efficacy and a similar rate of side effects compared to levonorgestrel emergency contraception, it is now recommended as first line treatment for emergency contraception. Emergency contraception is defined as the use of drug or device after unprotected or under-protected intercourse to prevent an unwanted pregnancy. Ulipristal acetate can be used up to 5 days (120 h) after unprotected sexual intercourse.
As progesterone promotes the growth of uterine fibroids, the blocking characteristic of ulipristal acetate can thereby be used to reduce the size of uterine fibroids. Ulipristal acetate has also shown efficacy with a significant reduction in uterine bleeding caused by uterine fibroids. The treatment of fibroids by ulipristal acetate should begin in the first week of a menstrual period.
Drugs or herbal products that induce enzymes, including CYP3A4, such as carbamazepine, phenytoin, rifampin, St. John's Wort, etc., may decrease the plasma concentrations of ulipristal acetate, and may decrease its effectiveness while CYP3A4 inhibitors such as itraconazole, ketoconazole, etc., may increase plasma concentrations of ulipristal acetate.
The half-life after oral intake is 32 h; it binds to plasma proteins for 97–99%, and it is metabolized by the citochrome P450.
Oral emergency contraception Ulinastal acetate is a new oral contraceptive pill, and it is the active chemical composition of Ella, a new generation of emergency contraceptive wildly on the market in United States currently. It can protect women within 120 hours after intercourse without medication, and the emergency contraceptive efficacy will not decline with the delay of treatment time. At the same time, it is safe and durable. Compared with the most commonly used emergency contraceptive levonorgestrel, Ulinastal acetate is more suitable for clinical use, and has the potential to prevent more unwanted pregnancies.
Ulipristal acetate was developed by HRA Pharmaceuticals, Inc., and was marketed by the Food and Drug Administration (FDA) in August 2010 under the trade name Ella. It could be used for the protection of unprotected sex or for the pregnancy prevention in the known or suspected contraceptive failure situation within 120h. Ulipristal acetate is a selective progesterone receptor modulator; and mainly it can take effect by inhibiting the ovulation and plays an emergency contraceptive effect. The study found that Ulastatal acetate was more effective than levonorgestrel in suppressing vomiting after dosing before the estimated ovulation day. And it consequently suggests that Ulatastatin acetate might have a stronger emergency contraceptive effectiveness.
the structure of ulcaritin acetate
Figure 1 for the structure of ulcaritin acetate
Pharmacological action Ulinastal acetate is a progesterone agonist/antagonist that inhibits or delays the ovulation; however, changes in the endometrium may also be a cause of efficacy.
Ulinastal acetate belongs to the category of selective progesterone receptor modulator, and it has partial agonistic action to progesterone receptor antagonism and partial agonism. It binds to progesterone receptors in the human body and prevents progesterone receptor binding. The efficacy of Ulinastal acetate depends on the time of administration in the menstrual cycle. Administration during the mid-follicular hyperplasia would suppress follicle formation and decrease the estradiol concentrations. And the administration during the in the peak period of follicular hyperplasia can delay the breakdown of follicles from 5 to 9 days. Although early luteal phase of administration cannot significantly delay the endometrial maturation, it can reduce the thickness of the endometrium within 0.6±2.2mm（average value ±SD）.