(R)-2-Fluor-α-methyl[1,1'-biphenyl]-4-essigsure

Danger

H301 (100%): Toxic if swallowed [Danger Acute toxicity, oral]

P264, P270, P301+P316, P321, P330, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 68 reports by companies from 3 notifications to the ECHA C&L Inventory.

MPC-7869 is not an inhibitor of cyclooxygenase enzymes (COX-1 and COX-2). The compound modulates the signal transduction and transcription activation pathways associated with nuclear factor kappaB (NFkappaB), a principle transcription factor in the expression of many molecules involved in cell growth, cell death and inflammation. In addition, MPC-7869 has recently been shown to modulate gamma-secretase and selectively lower levels of Abeta42 peptide in vitro and in vivo, and to reduce amyloid pathology in the brain. MPC-7869 has an excellent safety profile and is very potent in animal models of cancer and Alzheimer's disease. In transgenic mouse studies, MPC-7869 reduced brain amyloid levels and prevented memory loss.

Compounds capable of relieving pain without the loss of CONSCIOUSNESS.

Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions. They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects.

Agents that suppress GAMMA-SECRETASE by inhibiting or modulating its activities. Targeted enzymatic activities include its involvement in accumulation of toxic AMYLOID BETA-PEPTIDES (e.g., Aβ42) in ALZHEIMER DISEASE and activation of NOTCH RECEPTOR mediated SIGNAL PATHWAYS in certain cancer types.

Compounds or agents that combine with cyclooxygenase (PROSTAGLANDIN-ENDOPEROXIDE SYNTHASES) and thereby prevent its substrate-enzyme combination with arachidonic acid and the formation of eicosanoids, prostaglandins, and thromboxanes.