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To review the research progress of anticancer realgar preparations from the perspective of patent，in order to provide a reference for the research of new antitumor realgar drugs. IncoPat database was retrieved with keywords plus IPC classification number. Original data and 72 patents of anti-cancer realgar preparations were obtained and included after artificial denoising. The quantitative analysis was made on the information about application trends，application types and patentee. The technical points of representative patents were summarized. ① The patent types of anticancer realgar preparations are mainly product patents. Its technological innovation has undergone the development of realgar compound agents，arsenic sulfide single agents，nanometer products of realgar agents，bioleaching of realgar preparations，compound realgar extract preparations，compound nano realgar preparations and arsenic sulfide polymorphic crystalline structure. ② Nano realgar agents， realgar bioleaching preparations， new crystalline type realgar preparations and realgar compound preparations. ③ The following studies should be strengthened in the future，involving the comparison of biological effects and toxicity of nano realgar preparations of different preparation processes，the selection of optimal particle size，the druggability of realgar bioleaching preparations，the discovery of new As4S4 crystalline forms and the secondary development of anticancer realgar preparations.
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AIM: To explore the different effect and mechanism of arsenic sulfide on telemorase activity and hTERT-mRNA expression in CML cell lines-KS62 and APL cell lines-NB4. METHODS: Telomerase activity was determined by polymerase chain reaction enzyme-linked immunoassay (PCR-ELISA). The expression of hTERT-mRNA was analyzed by semi-quantitative RT-PCR. Flow cytometry was used to analyze the cell cycle and apoptosis. RESULTS: 0.15-0.6 mg/L arsenic sulfide (72 h)can induce apoptosis and inhibit telomerase activity and hTERT-mRNA expression in NB4 cell. The concentration of arsenic sulfide with the same effect on K562 cell was 0.3-3 mg/U 0.3 mg/L arsenic sulfide (72 h) can cause the proportion of the NB4 cell in G2/M phase increased, but for K562 cell, The concentration of arsenic sulfide was 1.5 mg/L. CONCLUSION: Telomerase system may be one.of the pathway for arsenic sulfide inducing apoptosis of NB4 and K562 cell; G2/M phrase arrest may have correlation with decrease of telomerase activity; The sensitivity of NB4 and K562 call for arsenic sulfide is different, the mechanism of it need to study more.
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AIM: To study if the effect of arsenic sulfide combined with IFN-α can be increased on K562 cells. METHODS: Telomerase activity was determined by PCRELISA. Flow cytometry was used to analyze the cell apoptosis. The final concentration of IFN-α and arsenic sulfide was 10 000 U/mL and 0.6 mg/L. RESULTS: The rates of apoptosis was 37.8% and 37% in K562 cells treated with IFN-α or arsenic sulfide alone for 8 days; The rates of apoptosis and inhibition of telomerase activity was 59.9% and 81.2% in K562 cells treated with IFN-α and arsenic sulfide simultaneously for 8 days, or 60.37% and 78.8% in K562 cells was treated with arsenic sulfide for 5 days after affected by IFN-α for 3 days. 71.3% telomerase activity was inhibited in K562 cells by arsenic sulfide alone for 8 days. CONCLUSION: Combination of arsenic sulfide and IFN-α can increase the apoptosis and inhibit the telomerase activity of K562 cells obviously comparing with the two drugs used alone. IFN-α maybe promote arsenic sulfide inducing apoptosis of K562 cells.