In general, the hydroxyl group makes alcohols polar. Those groups can form hydrogen bonds to one another and to most other compounds. 24034-73-9, formula is C20H34O, Owing to the presence of the polar OH alcohols are more water-soluble than simple hydrocarbons. Methanol, ethanol, and propanol are miscible in water. Butanol, with a four-carbon chain, is moderately soluble. Application of C20H34O
Chen, Ya-Hui;Huang, Ying-Chih;Yang, Shun-Fa;Yen, Hsu-Heng;Tsai, Horng-Der;Hsieh, Ming-Chia;Hsiao, Yi-Hsuan research published 《 Pitavastatin and metformin synergistically activate apoptosis and autophagy in pancreatic cancer cells》, the research content is summarized as follows. Pancreatic cancer is the seventh leading cause of cancer-related deaths globally. Metformin is the standard first-line of treatment for hyperglycemia in Type 2 diabetes, whereas pitavastatin is a cholesterol-lowering drug used to prevent cardiovascular diseases. Both these agents evidently exert anticancer effects on pancreatic cancer; however, it remains unclear whether cotreatment using them has additive or synergistic anticancer effects on pancreatic cancer. Thus, we herein used the ASPC-1 and PANC-1 cells and treated them with metformin and/or pitavastatin. We performed the cell viability assay, transwell migration assay, and cell cycle anal. using flow cytometry. Western blotting was used to determine protein levels. We found that cotreatment with metformin (30 mM) and pitavastatin (10μM) significantly reduced cell viability; caused G0/G1 cell cycle arrest; upregulated the expression levels of Bax, PCNA, cleaved PARP-1, cleaved caspase-3, LC3 II, and p27 Kip1/p21Cip1; and inhibited cell migration. The combination index value for cell viability indicated a synergistic interaction between metformin and pitavastatin. Moreover, cotreating the cells with metformin (30 mM) and pitavastatin (10μM) could preserve mitochondrial function, activate AMPK, and inhibit PI3K/mTOR than treatment with metformin or pitavastatin alone. These findings clearly indicated that metformin plus pitavastatin had a synergistic anticancer effect on pancreatic cancer cells, potentially caused due to the activation of AMPK and inhibition of PI3K/mTOR signaling. Altogether, our results provide that use of metformin plus pitavastatin maybe serve as a chemotherapeutic agent for human pancreatic cancer in future.
Application of C20H34O, Geranylgeraniol is a diterpenoid that is hexadeca-2,6,10,14-tetraene substituted by methyl groups at positions 3, 7, 11 and 15 and a hydroxy group at position 1. It has a role as a plant metabolite, a volatile oil component and an antileishmanial agent. It is a diterpenoid and a polyprenol.
Geranylgeraniol, a precursor to geranylgeranylpyrophosphate, is an intermediate in the mevalonate pathway. Geranylgeraniol has been shown to prevent bone re-absorption, inhibition of osteoclast formation, and kinase activation in vitro. When working with statins, Geranylgeraniol can reduce the toxicity without inhibiting the cholesterol-producing effects. Geranylgeraniol has been documented to counteract the effects of fluvastatin by inhibiting activation of caspase-1 and production of IL-1. Additionally Geranylgeraniol has been found to induce apoptosis in HL-60 cells.
, 24034-73-9.
Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts