Rubinotecan is a new semi synthetic camptothecin derivative. Preclinical pharmacological studies show that rubinotecan is a very ideal anti-tumor drug. It not only has a high inhibitory effect on common tumors, but also has a good synergistic effect with the currently commonly used anti-tumor drugs (such as 5-FU). It can also inhibit the recovery of sublethal damage. It can be used as a sensitizer for tumor radiotherapy. It can also inhibit the replication of HIV virus. It is also expected to be used in the treatment of acquired immunodeficiency syndrome in the future.

    Rupetecan is an oral preparation used by super Gen to treat pancreatic cancer and other solid tumors. The greatest advantage is that it can be taken during non hospitalization, so patients can be treated at home. Adverse reactions include: anemia, fatigue, cystitis, nausea, granulocytopenia, thrombocytopenia, vomiting, weight loss; Occasional constipation, diarrhea, fever, hematuria, infection, rash, gastrointestinal bleeding. No obvious heart, lung, liver, kidney and neurotoxicity. The toxic and side effects were dose-dependent and had no cumulative effect. They improved quickly after stopping or reducing the dosage. In conclusion, rupetecan is likely to become a new drug that has effects on a variety of tumors after taxol and gemcitabine. So, what is the anti-tumor mechanism of rubinotecan?

     RubitecanIts cytotoxic effect is mainly achieved by inhibiting Topo Ⅰ, an essential component of cell survival. Human Topo Ⅰ is a monomeric enzyme. Its main function is to relax DNA supercoiling. It plays an important role in DNA replication, transcription and recombination. Rubinotecan takes Topo Ⅰ as its target, but it does not kill cancer cells by inhibiting the catalytic activity of Topo Ⅰ, but by reversibly combining with TOPO Ⅰ -dna breaking complex to form drug Topo Ⅰ -dna ternary complex, which stabilizes the cleavable complex, forms a roadblock, makes the replication fork unable to proceed, and leads to cell death. Studies have shown that the content of Topo Ⅰ in a variety of tumor cells, especially colon cancer, cervical cancer and ovarian cancer, is much higher than that in normal tissues, especially in S-phase tumor cells. This may be one of the reasons for the good killing selectivity of ruticom. In addition, some studies have shown that the damage of RNA and DNA caused by short-term exposure to rubinotecan is reversible, but with the increase of concentration and the extension of exposure time, the inhibition of DNA progresses to non reversible, showing a two-way relationship between dose and practice.