Avicin D: Redox drug

Avicins’ effect on cancer and regular cell lines

The earliest experiments demonstrated potential in Jurkat T cells, Ovarian, and Pancreatic tumors, many of which are p53 null or mutant (red bars) (Mujoo et al., Cancer Research 61, 5486–5490, 2001).

Avicins induce cytotoxicity of myeloma cells.

Multiple myeloma (MM) remains incurable neoplasia, despite the recent development of several novel therapies. As part of our efforts to identify new compounds with anti-MM activity, we evaluated the class of Avicins, which are triterpenoid saponins that have been shown to induce apoptosis of neoplastic cells by affecting mitochondrial function independently of membrane-bound death receptors.

The Anticancer Plant Triterpenoid, Avicin D, Regulates Glucocorticoid Receptor Signaling

A model of Avicin D-GR interaction

Summary of toxicology in preclinical studies
- The weight loss observed at mid and high dose levels
- Liver and kidney are target organs based on clinical and histopathology findings
- Effects on liver, kidney, and weight are reversible
- Exposure level correlates with toxicity observed in both species: 100 – 400 ng/mL - correlates with mild to moderate, reversible toxicity

Safety Pharmacology

   Functional Observational Battery and Cardiovascular Safety/Respiratory Function

– No Findings

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