AECHL-1 targets breast cancer progression via inhibition of metastasis, prevention of EMT and suppression of Cancer Stem Cell characteristics.

Triple negative breast cancer (TNBC) features among the most aggressive manifestations of cancer due to its enhanced metastatic potential and immunity to therapeutics which target hormone receptors. Under such scenarios, anti-cancer compounds with an ability to influence multiple targets, or an entire process, will have an advantage over specific signal transduction inhibitors. To counter the metastatic threat it is essential to target cellular components central to the processes of cancer cell migration and adaptation.

Novel triterpenoid AECHL-1 induces apoptosis in breast cancer cells by perturbing the mitochondria-endoplasmic reticulum interactions and targeting diverse apoptotic pathways.

Background: The modus operandi for an anti-cancer drug must allow for an efficient discrimination system between tumorigenic and non-tumorigenic cells. Targeting ER stress and mitochondrial function in cancer cells appears to be a suitable option, as these processes are dysregulated in tumor cells. AECHL-1, a novel triterpenoid, exhibits potent anticancer activity against an array of cancer cell lines however, its mechanism of action remains elusive.

A novel SOD mimic with a redox-modulating mn (II) complex, ML1 attenuates high glucose-induced abnormalities in intracellular Ca transients and prevents cardiac cell death through restoration of mitochondrial function.

A key contributor to the pathophysiology of diabetic cardiomyopathy, mitochondrial superoxide can be adequately countered by Mn-superoxide dismutase, which constitutes the first line of defense against mitochondrial oxidative stress. Our group has recently synthesized low molecular weight SOD mimics, demonstrating superior protection against oxidative damages to kidney cells. In the current study, we sought to evaluate the protective effect of the SOD mimic ML1 against high glucose induced cardiomyopathy in diabetes.

AECHL-1, a novel triterpenoid, targets tumor neo-vasculature and impairs the endothelial cell cytoskeleton.

Tumor angiogenesis is characterized by abnormal vessel morphology leading to erratic and insufficient delivery of chemotherapeutics and oxygen, making the tumor core not only highly hypoxic but also unresponsive toward treatment. Such hypoxic conditions promote tumor aggressiveness, leading to the establishment of metastatic disease. Most anti-angiogenic treatments aim toward the destruction of tumor vasculature, which proves countereffective by further increasing its aggressive nature.