Significantly inhibit ovulation and prevent fertilized eggs from implanting, and increase the consistency of cervical mucus and the resistance of sperm penetration, thus playing a quick contraceptive role

This product is a fast-acting, short-acting contraceptive. Its contraceptive mechanism is to significantly inhibit ovulation and prevent the implantation of fertilized eggs, increase the viscosity of cervical mucus, and increase the resistance to sperm penetration, thereby exerting a fast-acting contraceptive effect.

This product is a fast-acting, short-acting contraceptive. Its contraceptive mechanism is to significantly inhibit ovulation and prevent the implantation of fertilized eggs, increase the viscosity of cervical mucus, and increase the resistance to sperm penetration, thereby exerting a fast-acting contraceptive effect.

This product is a fast-acting, short-acting contraceptive. Its contraceptive mechanism is to significantly inhibit ovulation and prevent the implantation of fertilized eggs, increase the viscosity of cervical mucus, and increase the resistance to sperm penetration, thereby exerting a fast-acting contraceptive effect.

Nicotinic acid is converted into nicotinamide in the body, and then combined with riboadenin to form nicotinamide adenine dinucleotide (coenzyme I) and nicotinamide adenine dinucleotide phosphate (coenzyme II), which are necessary for lipid amino acid, protein, purine metabolism, tissue respiration oxidation and glycogenolysis. Nicotinic acid can reduce the utilization of coenzyme A; by inhibiting the synthesis of very low density lipoprotein (VLDL), it affects the transport of cholesterol in the blood. Large doses can reduce serum cholesterol and triglyceride concentrations. Nicotinic acid has a peripheral vasodilation effect.

Ketoconazole is an azole antifungal drug. It has antibacterial and bactericidal effects on dermatophytes, yeasts (Candida, Pityrosporum, Torulopsis, Cryptococcus), dimorphic fungi and Fungi; except for Entomophthora, it has weaker effects on Aspergillus, Schenckia, some Phaeochromocytaceae, and Mucor. The mechanism of action of ketoconazole is mainly to highly selectively interfere with the activity of fungal cytochrome P-450, thereby inhibiting the biosynthesis of ergosterol on the fungal cell membrane.

This product is a piperazine calcium channel antagonist that can block calcium influx into vascular smooth muscle, causing vasodilation and improving cerebral and coronary circulation, especially having a certain selective effect on cerebral blood vessels. This product can inhibit phosphodiesterase, prevent cAMP from decomposing into inactive 5-AMP, thereby increasing the intracellular cAMP concentration, inhibiting the release of histamine, 5-hydroxytryptamine, bradykinin and other biologically active substances, and also inhibiting the activation of complement C4.

This product has a rapid effect and is one of the most potent topical corticosteroids currently used in clinical practice. It has a strong capillary constriction effect, and its anti-inflammatory effect is 112.5 times that of hydrocortisone, 2.3 times that of betamethasone sodium phosphate, and 18.7 times that of fluocinolone. The systemic adverse reactions are 3 times that of fluocinolone, and it has no sodium retention effect, and has a certain effect of promoting sodium and potassium excretion.