It stimulates K-opioid peptide receptors, has both agonist and antagonist effects on U-receptors, and indirectly exerts analgesic effects by interacting with receptors in the central nervous system; its effects on the central nervous system include reducing spontaneous breathing and coughing in the respiratory system, exciting the vomiting center, miosis, sedation, etc.; it may also achieve other effects through non-central nervous system mechanisms, such as changing the resistance and capacitance of heart vessels (nerves), regulating bronchial motor tension, affecting gastrointestinal secretion and motor muscle activity, and regulating bladder sphincter activity.

It stimulates K-opioid peptide receptors and has dual effects of stimulation and antagonism on U-receptors. Its pharmacological effects, including analgesia, are indirectly exerted through interactions with these receptors in the central nervous system. In addition to analgesia, the effects on the CNS include reducing spontaneous breathing of the respiratory system, coughing, exciting the vomiting center, miosis, sedation and other pharmacological effects. Its effects may be achieved through non-CNS mechanisms, such as changing the resistance and capacitance of cardiovascular (nerves), bronchial motor tension, gastrointestinal secretion, motor muscle activity and bladder sphincter activity. The analgesic effect of this product generally begins after a few minutes of intravenous injection and 10 to 15 minutes of intramuscular injection. It reaches its peak after 30 to 60 minutes of intravenous injection and intramuscular injection, and lasts for 3 to 4 hours, which is comparable to morphine, meperidine and pentazocine.

Docetaxel is a paclitaxel anti-tumor drug that exerts its anti-tumor effect by interfering with the microtubule network necessary for cell mitosis and interphase cell function. Docetaxel can bind to free tubulin, promote tubulin assembly into stable microtubules, and inhibit its depolymerization, resulting in the production of microtubule bundles that have lost their normal function and the fixation of microtubules, thereby inhibiting cell mitosis. The binding of docetaxel to microtubules does not change the number of protofilaments, which is different from most spindle toxic drugs currently used in clinical practice.