Resources

Resources:

Rivero-Cruz, J. F., et al. “Cytotoxic constituents of the twigs of Simarouba glauca collected from a plot in Southern Florida.” Phytother. Res. 2005; 19(2): 136-40.

Mata-Greenwood, E., et al. “Novel esters
of glaucarubolone as inducers of terminal differentiation of promyelocytic HL-60 cells and inhibitors of 7,12 dimethylbenz[a]anthracene- induced preneoplastic lesion formation in mouse mammary organ culture.” J. Nat. Prod. 2001; 64(12): 1509-13.
Morre, D. J., et al. “Mode of action of the anticancer quassinoids--inhibition of the plasma membrane NADH oxidase.” Life Sci. 1998; 63(7): 595-604. Valeriote, F. A., et al. “Anticancer activity of glaucarubinone analogues.” Oncol Res. 1998; 10(4): 201–8.
Ohno, N., et al. “Synthesis of cytotoxic fluorinated quassinoids.” Bioorg. Med. Chem. 1997; 5(8): 1489- 95.
Klocke, J. A., et al. “Growth inhibitory, insecticidal and antifeedant effects of some antileukemic and cytotoxic quassinoids on two species of agricultural pests.” Experientia. 1985 Mar 15; 41(3): 379-82. Handa, S. S., et al. “Plant anticancer agents XXV. Constituents of Soulamea soulameoides.” J. Nat. Prod. 1983; 46(3): 359–64.
Polonsky, J. “The isolation and structure of 13,18-dehydroglaucarubinone, a new antineoplastic quassinoid from Simarouba amara.” Experientia. 1978; 34(9): 1122–23.
Ghosh, P. C., et al. “Antitumor plants. IV. Constituents of Simarouba versicolor.” Lloydia. 1977; 40(4): 364–69.
Ogura, M. et al. “Potential anticancer agents VI. Constituents of Ailanthus excelsa (Simaroubaceae).” Lloydia. 1977; 40(6): 579–84.

Sinkcan demonstrates anti-inflammatory properties by reducing levels of IL4, IL5, IL13, Immunoglobin, INOS suppression, and COX2 inhibition. Moreover, it modulates the immune system through GB2 receptor activation and IL4 suppression, while also enhancing IFN gamma cytokine production.

In its approach to combating cancer, Sinkcan employs a dual strategy, aiming to disrupt cancer cell survival and growth while preserving healthy cells. Firstly, it targets glycolysis, a vital metabolic pathway for cancer cells, potentially improving chemotherapy effectiveness by sensitizing cancer cells. This strategy exploits cancer cells' reliance on glycolysis for energy, sparing healthy cells.

Secondly, Sinkcan triggers apoptosis, the self-destruction of cancer cells, and interferes with the cell cycle to hinder unchecked cell division. Additionally, it impedes cancer cell spread and angiogenesis, limiting metastasis. By integrating these mechanisms, Sinkcan offers a comprehensive cancer-fighting approach, addressing both cancer cell energy production and proliferation.

This amalgamation of traditional herbal remedies and modern medicine holds promise in enhancing cancer treatment outcomes while minimizing side effects.