This product is a lipid-regulating drug of the clofibric acid derivative class. Its mechanism of action in lowering blood lipids is not yet fully understood. It may involve peripheral fat decomposition, reduce the liver's uptake of free fatty acids and reduce the formation of triglycerides in the liver, inhibit the synthesis of very low-density lipoprotein apolipoproteins and reduce the production of very low-density lipoproteins. This product reduces blood triglycerides and increases blood high-density lipoprotein concentrations. Although it can slightly reduce blood low-density lipoprotein cholesterol blood concentrations, it may increase low-density lipoprotein in type IV hyperlipoproteinemia. A 5-year placebo-controlled study showed that this product can reduce the occurrence of severe coronary heart disease sudden death and myocardial infarction. Long-term administration of 10 times the human dose to rats increased the incidence of liver malignancies and benign testicular tumors.

Calcium blockers (also known as slow channel blockers or calcium antagonists) block the entry of calcium ions across the membrane into myocardial and vascular smooth muscle cells.

Telmisartan is an orally effective, specific angiotensin II receptor (AT1 type) antagonist. Telmisartan replaces angiotensin II receptors and binds to AT1 receptor subtypes with high affinity. It has no partial agonist effect at the AT1 receptor site, selectively binds to AT1 receptors and the binding effect is long-lasting. Telmisartan can cause a decrease in blood aldosterone levels, does not inhibit human plasma renin or ion channels, and does not inhibit angiotensin converting enzyme (kinase II), so there will be no adverse reactions caused by enhanced bradykinin action. Telmisartan can reduce systolic and diastolic blood pressure without affecting the pulse, and its antihypertensive effect is comparable to other types of representative antihypertensive drugs.

Rifampicin is a semi-synthetic broad-spectrum antibacterial drug of the rifamycin class, which has antibacterial activity against a variety of pathogenic microorganisms. The drug has a significant bactericidal effect on Mycobacterium tuberculosis and some non-tuberculous mycobacteria (including Mycobacterium leprae, etc.) both inside and outside the host cells. Rifampicin has a good antibacterial effect on aerobic Gram-positive bacteria, including enzyme-producing strains of Staphylococcus aureus and methicillin-resistant strains, Streptococcus pneumoniae, other Streptococcus, Enterococcus, Listeria, Bacillus anthracis, Clostridium perfringens, Corynebacterium diphtheriae, anaerobic cocci, etc. It also has a high degree of antibacterial activity against aerobic Gram-negative bacteria such as Neisseria meningitidis, Haemophilus influenzae, and Neisseria gonorrhoeae. Rifampicin also has a good effect on Legionella, and has an inhibitory effect on pathogens such as Chlamydia trachomatis, lymphogranuloma venereum, and psittacosis.

Amikacin sulfate is an aminoglycoside antibiotic that has good effects on most Enterobacteriaceae, Pseudomonas aeruginosa and some other Pseudomonas, Acinetobacter, Alcaligenes, etc. It also has good antibacterial effects on meningococci, gonococci, influenza bacilli, Yersinia, Campylobacter fetus, Mycobacterium tuberculosis and some Mycobacterium. Its antibacterial activity is slightly lower than that of gentamicin. Its most prominent advantage is that it is stable against aminoglycoside deactivating enzymes produced by many intestinal Gram-negative bacteria and will not lose its antibacterial activity due to deactivation of such enzymes. The mechanism of action is to act on the 30S subunit of bacterial ribosomes and inhibit bacterial protein synthesis. Combination with semi-synthetic penicillins or cephalosporins often achieves synergistic antibacterial effects.