LDCA

LDCA is a dual-hit metabolic modulator and inhibits LDH-A enzyme activity to stimulate apoptosis in the malignant population. LDCA can be used for the research of oncogenic progression[1].

Signaling Pathways >> Apoptosis >> Apoptosis

Research Areas >> Cancer

Signaling Pathways >> Metabolic Enzyme/Protease >> Lactate Dehydrogenase

LDCA is used in combination with doxorubicin synergistically enhances the growth inhibition and induces mitochondria-mediated apoptosis by recruiting the caspase cascade, restricting migration, and obviating the clonogenic outgrowth potential of melanoma cells[1]. Cell Viability Assay[1] Cell Line: B16-F10 cells Concentration: 2-100 μM Incubation Time: 72 h Result: Arrested cell growth with a dose-dependent cytotoxic effect and had a strong synergism with LDCA. Apoptosis Analysis[1] Cell Line: B16-F10 cells Concentration: 20 μM Incubation Time: 24 h Result: Resulted in 15% death when cells exposed to LDCA and caused 40% melanoma cell death combination synergistically with doxorubicin. Immunofluorescence[1] Cell Line: B16-F10 cells Concentration: 20 μM Incubation Time: 16 h Result: Demonstrated that combination with doxorubicin resultantly affected cellular morphology with condensed and fragmented nuclei. Cell Migration Assay [1] Cell Line: B16-F10 cells Concentration: 20 μM Incubation Time: 16 h Result: Signicantly limited the migratory potential in the B16-F10 cells.

LDCA (2 mg/kg, iv., the 6th day, once) is used in combination with doxorubicin thwarts tumor growth kinetics to restrain oncogenic progression, thus accentuating survival in the model of murine melanoma[1]. Animal Model: melanoma tumor model[1] Dosage: 2 mg/kg Administration: 2 mg/kg, iv., the 6th day, once Result: Significantly increased mice survivability combination with doxorubicin, and relieved mice tumor necrosis phenomena.

[1]. Saha, Suchandrima, et al. The dual-hit metabolic modulator LDCA synergistically potentiates doxorubicin to selectively combat cancer-associated hallmarks. RSC Advances, 7(84), 53322–53333. doi:10.1039/c7ra08625c.