Nocardamine

Nocardamine (NOCA) (0-20 μM; 24 h) shows no obvious cytotoxicity to periodontal ligament stem cells (PDLSCs), human dental pulp stem cells (DPSCs), human gingival fibroblasts (HGFs), and MC3T3-E1 preosteoblasts^[1].
Nocardamine (NOCA) (10 μM; 8 h) treatment on Pseudomonas aeruginosa PAO1 induces a log2 4.46-fold elevation in foxA transcription and a log2 6.37-fold increase in FoxA protein expression, with no significant regulatory effects on genes and proteins associated with pyocyanin-, pyocin-, or heme-dependent iron uptake pathways^[2].
Nocardamine drives ⁵⁵Fe uptake at a rate of 335.96 pmol/mL/OD600 nm, and this uptake process fully depends on the outer membrane transporter FoxA. Nocardamine only sustains the growth of Pseudomonas aeruginosa ΔpvdFΔpchA strains in iron-limited CAA medium, which confirms FoxA as the exclusive transporter responsible for iron-nocardamine complex uptake^[2].
Nocardamine is produced by Pseudomonas stutzeri (ATCC 17588). Its synthesis is inhibited by excessive Fe³⁺ (≥300 μg l^-1); it exhibits a biphasic response when the Fe³⁺ concentration is <200 μg l^-1, and forms a stable complex with Fe (III)^[3].
Nocardamine (1-100 μg/mL; 4 days) induces dose-dependent spindle-shaped morphological changes in BM-N4 insect cells; this activity is completely inhibited when the molar ratio of iron ions to Nocardamine is 2:1, and growth inhibition of P-388 or NB-1 mammalian cells occurs at a concentration of 100 μg/mL^[4].
Nocardamine (compound 5) exhibits cytotoxicity against Vero cells with an IC₅₀ of 16.57 µg/mL, while it shows no cytotoxic activity against KB, NCI-H187 or MCF-7 cell lines^[5].
Nocardamine (5-10 μM; pre-treatment for 4 hours followed by stimulation with 150 μM H₂O₂ for 24 hours) alleviates oxidative stress, reduces intracellular ROS accumulation, restores cell viability, restores the activities of SOD and CAT antioxidant enzymes inhibited by H₂O₂, and upregulates SIRT1 expression in a dose-dependent manner as well as restores p-ERK expression^[1].
Nocardamine (5-10 μM; pretreated for 4 hours, followed by stimulation with 150 μM H₂O₂ for 24 hours, and then osteogenic induction for 7/14 days) rescues the osteogenic differentiation capacity of PDLSCs damaged by oxidative stress, enhances ALP activity, promotes mineralized nodule formation, and upregulates the expression of osteogenic marker genes RUNX2, ALP, COL1A1 and their proteins^[1].
Nocardamine (10 μM; pretreated for 4 hours followed by stimulation with 150 μM H₂O₂ for 24 hours) increases the levels of β-catenin in the cytoplasm and nucleus of oxidative stress-induced PDLSCs^[1].

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