(Rac)-ZLc-002

(Rac)-ZLc-002, an inhibitor of nNOS interaction with nitric oxide synthase 1 adaptor protein (NOS1AP), suppresses inflammatory nociception and chemotherapy-induced neuropathic pain and synergizes with Paclitaxel (HY-B0015) to reduce tumor cell viability^[1][2]. IC50 & Target:nNOS/NOS1AP interaction^[1] In Vitro:(Rac)-ZLc-002 (10 μM) reduces co-immunoprecipitation of NOS1AP with nNOS immunoprecipitated from primary cultured cortical neurons. (Rac)-ZLc-002 fails to disrupt nNOS–NOS1AP protein–protein interactions in the AlphaScreen in vitro binding assay. It shows no activity in a cell-free assay^[1].
(Rac)-ZLc-002 (10 μM) reduces co-immunoprecipitation of full-length NOS1AP but not of PSD95-PDZ2 from HEK293T cells co-expressing full-length nNOS^[1].
(Rac)-ZLc-002 (0-50 μM; 72 h) synergizes with Paclitaxel (HY-B0015) to reduce tumor cell viability^[1]. In Vivo:(Rac)-ZLc-002 (10 mg/kg; i.p.; once or daily for 8 days) attenuates mechanical and cold allodynia evoked by Paclitaxel (HY-B0015), suppresses Paclitaxel-induced neuropathic pain in a mouse model^[1].
(Rac)-ZLc-002 (4 and 10 mg/kg; i.p.; once) reduces formalin-evoked nociceptive behavior and Fos-like immunoreactivity in the spinal dorsal horn in rats^[1].
(Rac)-ZLc-002 (40 mg/kg/day; i.v.; 7 days) attenuates chronic mild stress (CMS)‐induced anxiogenic behavior in ICR mice^[2].
(Rac)-ZLc-002 (10 μM; 1 μl; 30 min after Corticosterone, HY-B1618) delivering into the hippocampus for 7 days reverses the behavioural effects of glucocorticoids in mice^[2].