Biologically Active Small Molecules

A natural triterpene which stimulates wound healing induces cell cycle arrest and apoptosis in breast cancer cells (IC50 = 5.9 &microM for MCF-7 cells) blocks angiogenesis in glioblastomas down regulates BACE1 while increasing ADAM10 maturation

A natural triterpene which stimulates wound healing induces cell cycle arrest and apoptosis in breast cancer cells (IC50 = 5.9 &microM for MCF-7 cells) blocks angiogenesis in glioblastomas down regulates BACE1 while increasing ADAM10 maturation

The main saponin constituent of C. asiatica that has been shown to improve wound healing including increasing collagen synthesis and elevating antioxidant levels in various normal and diabetic wound models.

The main saponin constituent of C. asiatica that has been shown to improve wound healing including increasing collagen synthesis and elevating antioxidant levels in various normal and diabetic wound models.

The main saponin constituent of C. asiatica that has been shown to improve wound healing including increasing collagen synthesis and elevating antioxidant levels in various normal and diabetic wound models.

An asymmetric bis-pyridinium aldoxime that functions as an AChE reactivator through nucleophilic attack of oximate anions on organophosphate-AChE conjugates demonstrates therapeutic activity in experimental models of organophosphate poisoning.

An asymmetric bis-pyridinium aldoxime that functions as an AChE reactivator through nucleophilic attack of oximate anions on organophosphate-AChE conjugates demonstrates therapeutic activity in experimental models of organophosphate poisoning.

An asymmetric bis-pyridinium aldoxime that functions as an AChE reactivator through nucleophilic attack of oximate anions on organophosphate-AChE conjugates demonstrates therapeutic activity in experimental models of organophosphate poisoning.

An asymmetric bis-pyridinium aldoxime that functions as an AChE reactivator through nucleophilic attack of oximate anions on organophosphate-AChE conjugates demonstrates therapeutic activity in experimental models of organophosphate poisoning.

An ATP-competitive, second-generation ALK inhibitor (IC₅₀ = 3.5 nM) that also inhibits ROS (IC₅₀ = 8.

An ATP-competitive, second-generation ALK inhibitor (IC₅₀ = 3.5 nM) that also inhibits ROS (IC₅₀ = 8.

An ATP-competitive, second-generation ALK inhibitor (IC₅₀ = 3.5 nM) that also inhibits ROS (IC₅₀ = 8.