The growth of breast cancer cells can depend on the presence of estrogen. The estrogen (estrone and estradiol) in the circulation of postmenopausal women is mainly converted by aromatase in peripheral tissues from androgens (androstenedione and testosterone) in the adrenal glands and ovaries. Preventing estrogen production by inhibiting aromatase is an effective and selective method for treating postmenopausal hormone-dependent breast cancer. Exemestane is an irreversible steroid aromatase inactivator. It is similar in structure to androstenedione, the natural substrate of the enzyme, and is a pseudo-substrate of aromatase. It can inactivate the enzyme by irreversibly binding to its active site (this effect is also called self-destructive inhibition), thereby significantly reducing the level of estrogen in the blood circulation of postmenopausal women, but has no significant effect on the biosynthesis of corticosteroids and aldosterone in the adrenal glands. At a concentration 600 times higher than the concentration that inhibits aromatase, it has no significant effect on other enzymes in the steroidogenesis pathway.

It produces a local anesthetic effect by stabilizing nerve cell membranes by blocking the flow of ions required for the generation and conduction of nerve impulses.

It produces a local anesthetic effect by stabilizing nerve cell membranes by blocking the flow of ions required for the generation and conduction of nerve impulses.

Metronidazole has a strong antibacterial effect on most anaerobic bacteria, but has no effect on aerobic bacteria and facultative anaerobes. The antibacterial spectrum includes Bacteroides fragilis and other Bacteroides, Fusobacterium, Clostridium perfringens, Eubacterium, Veillonella, Peptococcus and Peptostreptococcus. Its bactericidal concentration is slightly higher than the inhibitory concentration. The bactericidal mechanism of metronidazole has not been fully elucidated. The nitroreductase of anaerobic bacteria plays an important role in the energy metabolism of sensitive strains. The nitro group of this product is reduced to a cytotoxin, thereby acting on the DNA metabolism process of bacteria and promoting cell death.

Meloxicam is a nonsteroidal anti-inflammatory analgesic (NSAID) of the enolic acid class, which has anti-inflammatory, analgesic and antipyretic effects. It exerts its pharmacological effects by inhibiting the biosynthesis of inflammatory mediators prostaglandins, and selectively inhibits COX-2 more strongly than COX-1, thereby reducing the incidence of gastrointestinal and renal side effects. Clinical studies have shown that when the recommended dose of meloxicam is used, the incidence of gastrointestinal adverse reactions (including perforation, ulcers or bleeding) is lower than that of other standard doses of NSAIDs.