Cloprostenol is a synthetic prostaglandin analogue structurally related to Prostaglandin F2α (PGF2α), for use in cattle and horses. As a potent luteolytic agent it causes functional and morphological regression of the corpus luteum (luteolysis) in cattle and horses followed by return to oestrus and normal ovulation.

Note: There is a refractory period of four to five days after ovulation when cattle and horses are insensitive to the luteolytic effect of prostaglandins. Cloprostenol has a good safety margin and does not impair fertility. No deleterious effects have been reported on the progeny conceived at the oestrus following treatment.

Cloprostenol is a synthetic prostaglandin analogue structurally related to Prostaglandin F2α (PGF2α). As a potent luteolytic agent, at dosage of only 500 micrograms, it causes functional and morphological regression of the corpus luteum (luteolysis) followed by return to oestrus and normal ovulation.

Corpus luteum regression is followed by a completely normal heat, from 2 to 4 days after administration in cows. No harmful effect has been shown on induced foetuses.

Pharmacological studies have shown that cloprostenol sodium is able to interrupt the pregnancy in rats, hamster and guinea pigs. The drug has no androgenic, estrogenic and anti-progestogen action, so its action is exclusively attributed to its luteolytic properties.

The molecule is more active when administered subcutaneously and in the most sensitive species, the pregnant hamster, it induces abortion with a dose of 1.25 mg/kg, compared to the dose of 25 mg/kg required by oral administration.

Cloprostenol sodium also induces abortion in pregnant animals with a mechanism still unknown.

At pharmacologically active doses, cloprostenol sodium does not induce symptoms of malaise in treated animals. Young rats, treated with a dose of 50 times the effective dose, presented signs of diarrhoea (adverse effects also observed in some monkeys under treatment).

Unlike other molecules similar to prostaglandins, cloprostenol sodium does not exert any thrombin-type action A2 and also does not cause platelet aggregation. Although the risk of infection at injection site caused by anaerobic bacteria may be increased due to the antithrombotic activity of some prostaglandin-similar molecules, the risk to be expected with cloprostenol sodium is that normally linked to any parenteral administration.

Studies of metabolism, using 15-14C-cloprostenol sodium, were conducted in swine and cattle (following I.M. administration) to determine residual levels. Studies have also been conducted in rats after subcutaneous administration.

The kinetic studies of cloprostenol sodium orally have not been conducted (route not relevant).

The drug's kinetic studies, conducted in both domestic animals and laboratory species, indicate that cloprostenol sodium is rapidly absorbed from the injection site. It is then metabolised and finally excreted practically similarly between urine and stool. In cattle and pigs the majority of the administered dose is excreted within 0-4 hours after injection and in practice the whole compound is excreted and metabolised within 24 hours.

The main pathway of metabolization in all animal species appears to be that of β-oxidation with formation of the tetranor or dinor acids of cloprostenol.

The values at the peak of radioactivity in the blood are observed within 1 hour of parenteral administration of sodium cloprostenol and tend to decrease with a T1/2 between 1 and 3 hours (depending on the animal species).