SERT/NET-IN-1 

SERT/NET-IN-1 is a blood-brain barrier-permeable SERT and NET inhibitor, with an IC₅₀ of 11.2 nM against human SERT and an IC₅₀ of 32.0 nM against human NET. SERT/NET-IN-1 blocks 5-HT reuptake to enhance serotonergic signaling. SERT/NET-IN-1 also blocks norepinephrine reuptake to enhance central noradrenergic transmission and inhibits the ejaculatory reflex. SERT/NET-IN-1 prolongs ejaculatory latency, reduces ejaculation frequency and preserves sexual function. SERT/NET-IN-1 exhibits cross-species microsomal metabolic stability, shows acceptable oral brain exposure in rats, and has favorable safety profiles. SERT/NET-IN-1 can be used in studies related to premature ejaculation^[1].

SERT/NET-IN-1 (compound 7) (1 μM; 0, 5, 15, 30, 60 min) exhibits excellent metabolic stability in human, mouse, rat, dog and monkey liver microsomes. The proportion of remaining parent compound ranges from 86.1% (rat) to 103% (dog) after 60 min, with 98.5% remaining in human liver microsomes^[1].
SERT/NET-IN-1 (100 μM; 48 h) shows no obvious cytotoxicity in either HEK293 or HepG2 cells, with an IC₅₀ of >100 μM in both cell lines^[1].
SERT/NET-IN-1 (100 μM; 48 h) exhibits almost no agonistic activity on μ-opioid receptors, with an EC₅₀ > 100 μM^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

SERT/NET-IN-1 (compound 7) (2.5 mg/kg, intravenous injection; 5 mg/kg, i.p.; 10 mg/kg, p.o.; single administration) exhibits the pharmacokinetic properties of rapid absorption (T_max=1.0 h) and moderate elimination (T_1/2=2.8 h) in Wistar rats. Its oral bioavailability reaches 61.60%, with an AUC_0-t of 1347.05 ng?h/mL; the brain concentration reaches 143 ng/g at 0.5 h post-administration, with a brain/plasma ratio of 0.45; the brain concentration reaches 152.33 ng/g at 4 h post-administration, with the brain/plasma ratio increasing to 1.96, indicating favorable blood-brain barrier penetration ability^[1].
SERT/NET-IN-1 (20 mg/kg; i.p.; single administration, tested 15 min post-dose) significantly prolongs the ejaculation latency period (from 223.3 s to 713.2 s) and reduces the number of ejaculations within 20 min (from 2.25 to 1.125) in the 8-OH-DPAT-induced premature ejaculation model of male Wistar rats^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

288.41

C₁₆H₂₀N₂OS

CCC(N(C1CCNCC1)C2=C3C=CSC3=CC=C2)=O

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Cui W, et al. N-aryl-N-acyl diamine derivatives as novel selective serotonin/norepinephrine transporter inhibitors for the treatment of premature ejaculation. Eur J Med Chem. Published online March 20, 2026.