Biologically Active Small Molecules

An immediate precursor of cholesterol elevated in the neurodevelopmental syndrome Smith-Lemli-Opitz syndrome, where it is subject to free radical oxidation, giving rise to several oxysterols which contribute to pathogenesis converted by

An immediate precursor of cholesterol elevated in the neurodevelopmental syndrome Smith-Lemli-Opitz syndrome, where it is subject to free radical oxidation, giving rise to several oxysterols which contribute to pathogenesis converted by

An immediate precursor of cholesterol elevated in the neurodevelopmental syndrome Smith-Lemli-Opitz syndrome, where it is subject to free radical oxidation, giving rise to several oxysterols which contribute to pathogenesis converted by

An immediate precursor of cholesterol elevated in the neurodevelopmental syndrome Smith-Lemli-Opitz syndrome, where it is subject to free radical oxidation, giving rise to several oxysterols which contribute to pathogenesis converted by

The inactive 7(S) epimer of Maresin 1 useful as an experimental negative control.

The inactive 7(S) epimer of Maresin 1 useful as an experimental negative control.

The inactive 7(S) epimer of Maresin 1 useful as an experimental negative control.

The inactive 7(S) epimer of Maresin 1 useful as an experimental negative control.

A fluorophore used to monitor functional activity of CYP1A1, CYP2B4, and CYP2B6 excitation/emission maxima equals 318 and 377 nm, respectively in methanol and 360 and 449 nm, respectively in dealkylase.

A fluorophore used to monitor functional activity of CYP1A1, CYP2B4, and CYP2B6 excitation/emission maxima equals 318 and 377 nm, respectively in methanol and 360 and 449 nm, respectively in dealkylase.

A fluorophore used to monitor functional activity of CYP1A1, CYP2B4, and CYP2B6 excitation/emission maxima equals 318 and 377 nm, respectively in methanol and 360 and 449 nm, respectively in dealkylase.

A fluorometric substrate for and competitive inhibitor of cytochrome P450 1A1 used to study the metabolism of arachidonic acid and the mechanisms of vasodilation inhibits nitric oxide synthesis by uncoupling nNOS (Ki = 0.76 &microM).