Fluoxetine, Hydrochloride

A cell-permeable phenylpropylamine derived anti-depressant that acts as a selective serotonin re-uptake inhibitor (SSRI). Reported to modulate the proliferation of T cells by increasing the Ca²⁺ influx thereby influencing the activities of protein kinase A (PKA) and protein kinase C (PKC). Inhibits leak K⁺ currents in a reversible and voltage-independent manner (IC₅₀ = 780 nM). Also shown to regulate the phosphorylation of DARPP-32 (dopamine-and cAMP-regulated phosphoprotein of Mr 32,000) and AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptors. Triggers oxidative stress-induced apoptotic cell death and initiates signaling pathways in neuronal cells leading to an activation of ERK and NF-κB.

A cell-permeable phenylpropylamine derived anti-depressant that acts as a selective serotonin re-uptake inhibitor (SSRI). Reported to modulate the proliferation of T-cells by increasing the Ca²⁺ influx and thereby influencing the activities of protein kinase A (PKA) and protein kinase C (PKC). Also shown to regulate the phosphorylation of DARPP-32 (dopamine-and cAMP-regulated phosphoprotein of M_r 32,000) and AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptors. Shown to trigger oxidative stress-induced apoptotic cell death. Also reported to initiate signaling pathways in neuronal cells leading to activation of ERK and NF-κB.

Cell permeable: yes

Primary Target
Selective serotonin re-uptake inhibitor

Product does not compete with ATP.

Reversible: no

Packaged under inert gas

Toxicity: Harmful (C)

Following reconstitution aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.

Bartholoma, P., et al. 2002. Biochem. Pharmacol.63, 1507.
Bian, J.T., et al. 2002. Eur. J. Pharmacol.453, 159.
Zhang, A., et al. 2002. J. Med. Chem.45, 1930.
Svenningsson, P., et al. 2002. Proc. Natl. Acad. Sci. USA99, 3182.
Edgar, V.A., et al. 1999. Eur. J. Pharmacol.372, 65.

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