Biologically Active Small Molecules

The inactive enantiomer of the SET7/9 inhibitor (R)-PFI-2 that may serve as a negative control.

The inactive enantiomer of the SET7/9 inhibitor (R)-PFI-2 that may serve as a negative control.

The inactive enantiomer of the SET7/9 inhibitor (R)-PFI-2 that may serve as a negative control.

A potent and selective CB1 receptor antagonist (Kis = 7.8 and 7,943 nM for CB1 and CB2, respectively) less lipophilic (log P = 5.1) and therefore more water soluble than other known CB1 receptor ligands.

A potent and selective CB1 receptor antagonist (Kis = 7.8 and 7,943 nM for CB1 and CB2, respectively) less lipophilic (log P = 5.1) and therefore more water soluble than other known CB1 receptor ligands.

A potent and selective CB1 receptor antagonist (Kis = 7.8 and 7,943 nM for CB1 and CB2, respectively) less lipophilic (log P = 5.1) and therefore more water soluble than other known CB1 receptor ligands.

A synthetic intermediate useful for pharmaceutical synthesis.

A major phase I metabolite of tamoxifen, a well-known estrogen receptor antagonist in breast but partial estrogen receptor agonist in endometrium has at least a 100-fold higher affinity for estrogen receptors than tamoxifen.

A major phase I metabolite of tamoxifen, a well-known estrogen receptor antagonist in breast but partial estrogen receptor agonist in endometrium has at least a 100-fold higher affinity for estrogen receptors than tamoxifen.

A major phase I metabolite of tamoxifen, a well-known estrogen receptor antagonist in breast but partial estrogen receptor agonist in endometrium has at least a 100-fold higher affinity for estrogen receptors than tamoxifen.

A major phase I metabolite of tamoxifen, a well-known estrogen receptor antagonist in breast but partial estrogen receptor agonist in endometrium has at least a 100-fold higher affinity for estrogen receptors than tamoxifen.

An analog of GlcNAc that reversibly inhibits NCOAT (O-GlcNAcase).