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Allopathic Medicines
Published in Varma H. Rambaran, Nalini K. Singh, Alternative Medicines for Diabetes Management, 2023
Varma H. Rambaran, Nalini K. Singh
Other examples of biguanides, such as phenformin (Figure 2.3a) and buformin (Figure 2.3b), were marketed in the United States in the 1950s, subsequently becoming available across Canada, the United Kingdom, and Australia. However, these were removed from the market in the 1970s because of the toxic events that they were associated with in the body (Bailey 1992, Wang and Hoyte 2019). Additionally, metformin toxicity has also been known to lead to hyperlactatemia and metabolic acidosis, though the level of incidence is very low due to its acceptable level of excretion (Wang and Hoyte 2019).Structures of examples of biguanides: (a) phenformin and (b) buformin.
Substrates of Human CYP2D6
Published in Shufeng Zhou, Cytochrome P450 2D6, 2018
Oral hypoglycemic drugs include the sulfonylureas (e.g., glipizide, glimepiride, and glyburide) and biguanides (e.g., met-formin, buformin, and phenformin), which are currently used in the treatment of type II diabetes (Marchetti et al. 1991).
Autophagy: The Way to Death or Immortality? Activators and Inhibitors of Autophagy as Possible Modulators of the Aging Process
Published in Shamim I. Ahmad, Aging: Exploring a Complex Phenomenon, 2017
Galina V. Morgunova, Alexander A. Klebanov, Alexander N. Khokhlov
Equally popular is metformin, a drug long used in the treatment of diabetes (Anisimov et al. 2008; Smith et al. 2010; Martin-Montalvo et al. 2013). The choice of this drug as a CRM is completely logical since diabetes and obesity (usually, a result of overnutrition) are related issues, and therefore, the medicine against the first should, to some extent, also help from the second. Metformin and other biguanides (buformin and phenformin) probably can indeed activate autophagy, but data on the effect of these compounds on healthy (nondiabetic) animals is still insufficient (Anisimov 2010, 2013). The mechanism of action of biguanides is associated with the activation of AMPK (AMP-activated protein kinase) (Zhou et al. 2001). AMPK is a sensor that reacts to a lack of energy, which is expressed in an increase in the ratio of AMP/ATP. Metformin activates AMPK, and it, in turn, inhibits TOR and takes the cell into an “economical” mode of existence.
Acid-base and electrolyte disturbances in patients with diabetes mellitus
Published in Acta Clinica Belgica, 2019
Lissa Pipeleers, Karl Martin Wissing, Robert Hilbrands
A severe side-effect of biguanides is the development of lactic acidosis, which has led to the withdrawal of two older biguanides (phenformin and buformin) from the market many years ago [9]. The risk of lactic acidosis is much lower with metformin, with an estimated incidence ranging from 1 to 16.7 cases per 100,000 patient years of treatment [13,14]. The significance of lactic acidosis as a side effect of metformin was even questioned by two systematic reviews in which the incidence of metformin-associated lactic acidosis (MALA) was not distinguishable from the background rate of lactic acidosis in the overall population with diabetes [15,16].
A dual-functional buformin-mimicking poly(amido amine) for efficient and safe gene delivery
Published in Journal of Drug Targeting, 2020
Mei Lu, Haonan Xing, Lin Cheng, Hui Liu, Lang Lang, Tianzhi Yang, Xiaoyun Zhao, Hui Xu, Pingtian Ding
Biguanides including metformin, phenformin and buformin have long been used in the treatment of type-2 diabetes. In addition to their antihyperglycemic effect, biguanides have been reported to be capable of reducing the risk of cancer and tumorigenesis through activation of AMPK and inhibition of mTOR pathways in multiple types of neoplasms [19–21]. Therefore, in the following section, cell viability and western-blot analysis were performed to explore whether buformin-mimicking side chains could endow CBA-Bu with antiproliferative effects on cancer cells through pathways similar to that of buformin.