It can reduce the increase of serum AST and ALT in the animal acute liver injury model caused by TAA (thioacetamide) and CC14 (carbon tetrachloride), and inhibit the accumulation of triglycerides caused by chronic liver injury model; it can promote liver glycogen synthesis, inhibit the increase of cholesterol, and help to restore the serum albumin/globulin ratio.

Gabexate is a non-peptide protease inhibitor that can inhibit the activity of proteases such as trypsin, kallikrein, plasmin, and thrombin, thereby preventing the pathological and physiological changes caused by these enzymes.

It is relatively stable against beta-lactamase produced by Staphylococcus aureus and has a strong antibacterial effect on Gram-positive bacteria. It has the same activity as cefoperazone against penicillinase-producing Staphylococcus aureus, group A hemolytic streptococci, grass-green streptococci and Staphylococcus epidermidis, and is 2-4 times stronger than cefoperazone against non-enzyme-producing Staphylococcus aureus and pneumococci. It is more active than cefoperazone against Gram-negative bacilli including Escherichia coli and Klebsiella pneumoniae, and is similar to cefoperazone. It is more active than cefoperazone against Proteus mirabilis, Salmonella and Shigella. It can inhibit all influenza bacilli, including ampicillin-resistant strains. Moraxella catarrhalis and gonococci are sensitive to this product. Indole-positive Proteus, Serratia, Acinetobacter and Pseudomonas aeruginosa are all resistant to cefoperazone.

It has a strong effect of dissolving mucus and can break down the polysaccharide cellulose in sputum and thin the sputum. It inhibits the synthesis of glycoproteins by goblet cells and mucous glands to reduce the sialic acid in sputum, reduce the viscosity of sputum, and facilitate discharge.

In vitro tests have destructive or inhibitory effects on the morphology or proliferation of cell lines such as liver cancer, esophageal cancer, laryngeal cancer, lung cancer, and cervical cancer; in vivo tests have a certain inhibitory effect on Ehrlich ascites carcinoma, sarcoma-180 and solid liver cancer in mice, and can increase the respiratory control rate and lysosomal enzyme activity of mitochondria in ascites liver cancer H22 mice, interfere with cancer cell division, block it in the M phase, and affect its cycle speed; destroy the cancer cell skeleton (microfilaments, microtubules), affect the ultrastructure of cancer cells, and cause damage to mitochondria, microvilli and plasma membranes; can inhibit cancer cell DNA synthesis, but has no inhibitory effect on normal bone marrow cells, and can increase white blood cells.

It binds to the target protein on the cell membrane, making it impossible for the bacteria to maintain their normal form and normal division and reproduction, and finally lyses and dies. It is extremely stable to β-lactamase, has strong antibacterial activity against Gram-negative bacteria and anaerobic bacteria, has a slightly weaker effect on Gram-positive bacteria, and also has a certain antibacterial effect on Pseudomonas aeruginosa.