Tyrosine kinase inhibitor, indicated for the treatment of patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) who have been tested for epidermal growth factor receptor (EGFR) gene sensitive mutations.

Gefitinib is a reversible inhibitor of wild-type and certain mutant EGFRs, which inhibits EGFR receptor tyrosine autophosphorylation, thereby further inhibiting downstream signal transduction and preventing EGFR-dependent cell proliferation. Gefitinib has a greater affinity for mutant EGFR (exon 19 deletion and exon 21 L858R mutation) than for wild-type EGFR. Gefitinib can also inhibit IGF- and PDGF-mediated signal transduction at clinically relevant concentrations; the inhibitory effect of gefitinib on other tyrosine kinases is not yet clear.

Pregabalin has a high affinity for the α2-δ site (an auxiliary subunit of voltage-gated calcium channels) in the central nervous system. It may reduce the calcium-dependent release of some neurotransmitters by regulating calcium channel function. Pregabalin does not directly bind to GABAA, GABAB or benzodiazepine receptors, does not increase the GABAA response of neurons cultured in vitro, does not change the GABA concentration in rat brain, and has no acute effect on GABA uptake or degradation. Pregabalin does not block sodium channels, has no activity on opioid receptors, does not change cyclooxygenase activity, has no activity on dopamine and 5-hydroxytryptamine receptors, and does not inhibit the reuptake of dopamine, 5-hydroxytryptamine or norepinephrine.

By binding to the CysLT1 receptor, it inhibits the physiological effects of LTC4, LTD4 and LTE4, and improves asthma inflammation indicators. It has high affinity and selectivity for the CysLT1 receptor and has no receptor agonist activity. It is used to relieve asthma symptoms and allergic rhinitis symptoms.

Palonosetron is a selective antagonist of the 5-HT3 receptor with strong affinity, and has no affinity or low affinity for other receptors. The 5-HT3 receptor is located in the vagus nerve endings in the central and peripheral emetic chemotherapy receptor area of the medulla oblongata. Chemotherapy drugs stimulate the release of 5-HT by chromaffin cells in the small intestine, and 5-HT then activates the 5-HT3 receptors of the vagal afferent nerves, producing a vomiting reflex.