FGIN 1-27

FGIN-1-27 is a blood-brain barrier-penetrant TSPO ligand with a K_i value of 5 nM. FGIN 1-27 inhibits PKC-β, PKA/CREB, p38/ERK MAPK, MITF, tyrosinase, TRP-1, and TRP-2, thereby inhibiting melanogenesis and pigmentation. FGIN-1-27 alleviates X-ray radiation-induced astrocyte mitochondrial hyperfunction, reduces ROS and superoxide production, inhibits excessive activation of A1-type astrocytes, downregulates GFAP and C3 protein expression, and restores astrocyte proliferative capacity. FGIN-1-27 produces anticonvulsant effects in normal mice; in diazepam-withdrawn mice, the brain MDR pathway becomes subsensitive, and the anticonvulsant activity disappears. FGIN-1-27 attenuates pigmentation in zebrafish embryos and ameliorates UVB-induced skin pigmentation in guinea pigs. FGIN-1-27 directly stimulates testicular Leydig cells while upregulating luteinizing hormone levels, causing an acute increase in serum testosterone in male rats. FGIN 1-27 can be used for research related to hyperpigmentation, epilepsy, brain injury, and other diseases^{[1][2][3][4][5]}. In Vitro:FGIN-1-27 (10 min) does not directly inhibit mushroom tyrosinase activity in cell-free assays^[1].
FGIN-1-27 (1-16 μM; 48 h) does not reduce the viability of SK-MEL-2 cells or HEM^[1].
FGIN-1-27 (1-4 μM; 48 h) inhibits basal and α-MSH (HY-P0252)-, OAG-, or ET-1-induced melanin synthesis in SK-MEL-2 cells and HEM^[1].
FGIN-1-27 (0-4 μM; 48 h) inhibits tyrosinase, TRP-1, and TRP-2 expression in SK-MEL-2 cells and HEM, and inhibits OAG-induced cellular tyrosinase activity^[1].
FGIN-1-27 (4 μM; 1-12 h) inhibits basal, α-MSH-induced, and ET-1-induced MITF expression in SK-MEL-2 cells and HEM^[1].
FGIN-1-27 (4 μM; 0-120 min) reduced PKC-β, p-PKA cat, p-CREB, p-p38, and p-ERK protein levels in SK-MEL-2 cells and HEM^[1].
FGIN 1-27 (40 μM; 2 h) stimulates testosterone production in primary rat Leydig cells through a PKA-sensitive mechanism at or downstream of mitochondrial steroidogenesis, without requiring calcium signaling or new protein synthesis, and without altering the mRNA levels of key steroidogenic genes^[3].
FGIN-1-27 (1 μM; 24 h) reduced GFAP/C3 expression and restored EdU-positive proliferation in primary C57BL/6 mouse astrocytes exposed to 20 Gy X-rays without altering viability; it also stabilized mitochondrial membrane potential and reduced mitochondrial hyperrespiration and oxidative stress^[5].
FGIN-1-27 (10 µM; 6 days) selectively inhibits the proliferation of conventional CD4⁺ T cells, CD8⁺ T cells, Th1, and Th17 subsets in phytohemagglutinin-stimulated human PBMCs and reduces IL-17A and IFN-γ production while preserving Treg proliferation^[4]. In Vivo:FGIN-1-27 (1%; topical administration; twice daily; 3 weeks) reduces UVB-induced skin hyperpigmentation in guinea pigs without reducing melanocyte numbers^[1].
FGIN-1-27 (20-30 μg/mouse; i.c.v.; single administration 15-30 min before PTZ infusion) increases the pentylenetetrazol seizure threshold in chronically vehicle-treated ddY mice; it does not increase the seizure threshold in benzodiazepine-withdrawn mice^[2].
FGIN 1-27 (1 μg/g body weight (1 mg/kg BW); i.p.; single dose) acutely increases serum testosterone in healthy adult male SD rats; it also increases serum LH at 2 h without altering serum FSH^[3].