5-(3',4'-Dihydroxyphenyl)-γ-valerolactone

5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (VL) (1.5-50 µM; 6-48 h) shows no cytotoxic effects on LS174T, HepG2, Caco2, or Wt-MDCK cells^[1].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (50 µM; 120 min) is rapidly converted to its sulfate conjugate (VLS) in Caco2 and Wt-MDCK cell monolayers; VLS exhibits high apparent permeability in both models, with efflux transporter involvement indicated by an efflux ratio >2 in Caco2 cells^[1].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (1.5-50 µM; 90 min for inhibition assays; 2.5-10 µM; 48 h for induction assays), as its sulfate conjugate VLS, mildly activates the BCRP efflux transporter in differentiated Caco2 cells at concentrations of 12.5 to 50 µM, but does not modulate P-gp activity at tested concentrations^[1].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (10 µM; up to 120 min) is rapidly metabolized via phase II glucuronidation in human liver S9 fraction (t_1/2 = 8.72 min) and more slowly via phase I metabolism in human liver microsomes (t_1/2 = 23.08 min), forming two glucuronide conjugates as primary hepatic metabolites^[1].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (DHPV) (5-100 μM; 36 h) promotes proliferation of MC3T3-E1 preosteoblast cells and attenuates H₂O₂-induced cytotoxicity in MC3T3-E1 cells when used at 5-15 μM for 36 h pretreatment followed by 48 h H₂O₂ exposure^[3].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (5-15 μM; 36 h pretreatment, followed by 48 h H₂O₂ exposure, then up to 14 days in differentiation medium) attenuates H₂O₂-induced inhibition of osteogenic differentiation in MC3T3-E1 preosteoblast cells, restoring ALP and Runx2 expression, ALP activity, and mineralization capacity^[3].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (5-15 μM; 36 h pretreatment, followed by 48 h H₂O₂ exposure) protects MC3T3-E1 preosteoblast cells from H₂O₂-induced mitochondrial membrane potential loss, with 15 μM exerting a significant restorative effect^[3].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (5-15 μM; 36 h pretreatment, followed by 48 h H₂O₂ exposure) alleviates H₂O₂-induced oxidative stress in MC3T3-E1 preosteoblast cells, reducing ROS and MDA levels and restoring SOD activity, with 15 μM exerting significant effects across all measured parameters^[3].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (5-15 μM; 36 h pretreatment, followed by 48 h H₂O₂ exposure) enhances autophagy in H₂O₂-treated MC3T3-E1 preosteoblast cells via increased LC3-II/I and Beclin-1 expression, with 15 μM exerting a more potent effect^[3].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (15 μM; 36 h pretreatment, followed by 48 h H₂O₂ exposure) upregulates SIRT1 protein expression in MC3T3-E1 preosteoblast cells, reversing H₂O₂-induced suppression of SIRT1^[3].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (5-15 μM; pretreatment following SIRT1 siRNA transfection, followed by 48 h H₂O₂ exposure) preserves mitochondrial membrane potential in SIRT1-silenced, H₂O₂-treated MC3T3-E1 preosteoblast cells, indicating its protective effect on mitochondrial function is mediated via SIRT1^[3].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (5-15 μM; pretreatment following SIRT1 siRNA transfection, followed by 48 h H₂O₂ exposure) mitigates oxidative stress in SIRT1-silenced, H₂O₂-treated MC3T3-E1 preosteoblast cells, indicating its antioxidant effects are mediated via SIRT1^[3].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (5-15 μM; pretreatment following SIRT1 siRNA transfection, followed by 48 h H₂O₂ exposure) enhances autophagy in SIRT1-silenced, H₂O₂-treated MC3T3-E1 preosteoblast cells, indicating its autophagy-promoting effect is mediated via SIRT1^[3].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (5-15 μM; pretreatment following SIRT1 siRNA transfection, followed by 48 h H₂O₂ exposure, then up to 14 days in differentiation medium) restores osteogenic differentiation capacity in SIRT1-silenced, H₂O₂-treated MC3T3-E1 preosteoblast cells, indicating its pro-osteogenic effect is mediated via SIRT1^[3].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (DHPV) (5-20 μM; duration of adipogenesis differentiation) does not reduce viability of 3T3-L1 preadipocytes at concentrations up to 20 μM^[4].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (120 minutes) directly inhibits CDK2/cyclin O kinase activity with an IC₅₀ of 8.79 μM^[4].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (2 mg; overnight at 4°C) directly binds to the CDK2/cyclin O complex in vitro^[4].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (γ-VL) (1-100 μM; 24 h) is non-cytotoxic to primary rat cortical microglia at concentrations from 1 to 50 μM, but induces significant cytotoxicity at 100 μM^[6].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (𝛾VL) (1-500 μM; 0-60 min) is subject to calcium²⁺-dependent hydrolysis catalyzed by pooled male human serum paraoxonase to γ-valeric acid, with an apparent substrate half-life of 9.8 min and a Michaelis-Menten constant (K_m) of 269 μM^[9].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (1 μM; 1 h) undergoes calcium²⁺-dependent hydrolysis catalyzed by PON1 and PON3 (but not PON2) expressed in HEK293FT cells to γ-valeric acid, matching activity observed in pooled human serum^[9].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (1 μM; 1 h) has specific phase II metabolites that are selectively hydrolyzed by pooled male human serum paraoxonase, with γVL-3'-methoxy-4'-glucuronide, γVL-4'-glucuronide, and γVL-3'-sulfate being the most reactive substrates^[9].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (DHPV) (7.5-30 μM; 1 h pretreatment; 5 h TNF-α stimulation) concentration-dependently inhibits TNF-α-stimulated adhesion of THP-1 monocytes to HUVECs, with significant inhibition observed at concentrations as low as 7.5 μM, and does not reduce HUVEC viability at concentrations up to 30 μM^[2].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (7.5-30 μM; 1 h pretreatment; 5 h TNF-α stimulation (protein analysis); 4 h TNF-α stimulation (mRNA analysis)) concentration-dependently downregulates TNF-α-stimulated VCAM-1 protein and mRNA expression in HUVECs, with significant suppression observed at concentrations as low as 7.5 μM^[2].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (7.5-30 μM; 1 h pretreatment; 5 h TNF-α stimulation (protein secretion analysis); 4 h TNF-α stimulation (mRNA analysis)) concentration-dependently reduces TNF-α-stimulated MCP-1 protein secretion and MCP-1 mRNA expression in HUVECs, with significant suppression observed at concentrations as low as 7.5 μM^[2].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (7.5-30 μM; 1 h pretreatment; 10 h TNF-α stimulation) concentration-dependently inhibits TNF-α-stimulated NF-κB transcriptional activation in stably transfected HUVECs, with significant suppression observed at concentrations as low as 7.5 μM^[2].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (7.5-30 μM; 1 h pretreatment; 15 min TNF-α stimulation) concentration-dependently suppresses TNF-α-stimulated phosphorylation of IKK and IκBα, and prevents IκBα degradation, in HUVECs, with significant inhibition observed at concentrations as low as 7.5 μM^[2].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (5-20 μM; 6 days) dose-dependently reduces MDI-induced intracellular lipid accumulation in 3T3-L1 preadipocytes, with maximal inhibition at 20 μM reducing lipid content to ~72% of MDI-only control levels^[4].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (5-20 μM; duration of adipogenesis differentiation) dose-dependently reduces expression of adipogenic (PPAR γ, C/EBP α) and lipogenic (SREBP1c, ACC, FAS) proteins in MDI-induced 3T3-L1 preadipocytes^[4].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (5-20 μM; duration of adipogenesis differentiation) dose-dependently reduces MDI-induced phosphorylation of C/EBP β at Thr 188 in 3T3-L1 preadipocytes^[4].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (20 μM; days 0-2 of differentiation) most potently inhibits MDI-induced adipogenesis in 3T3-L1 preadipocytes when applied during the early 0-2 day mitotic clonal expansion stage^[4].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (DHPV) (5-20 μM; 3-4 days) reduces lipid accumulation in mature 3T3-L1 adipocytes by suppressing lipogenic protein expression, without affecting lipolysis^[4].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (20 μM; 16 hours of differentiation) induces G1 phase arrest, delaying MDI-induced cell cycle progression from G1 to S phase in 3T3-L1 preadipocytes^[4].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (1-50 μM; 1 h pre-incubation, followed by 24 h LPS stimulation) inhibits LPS-induced release of IL-1β, TNF-α, and NO in primary rat cortical microglia, with significant effects starting at 25 μM for IL-1β and TNF-α, and 50 μM for NO^[6].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (1-25 μM in combination with 1-5 μM curcumin; 1 h pre-incubation, followed by 6 or 24 h LPS stimulation) synergizes with Curcumin (HY-N0005) to reduce LPS-induced pro-inflammatory gene expression and mediator release in primary rat cortical microglia, with ZIP model synergy scores ranging from 16.07 to 28.18 for key pro-inflammatory mediators^[6].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (5 μM in combination with 5 μM curcumin; 1 h pre-incubation, followed by 6 h LPS stimulation) synergizes with curcumin at 5 μM each to downregulate LPS-induced NLRP3 and NOX2 expression, and upregulate Nrf2 target genes HO-1 and NQO-1, in primary rat cortical microglia^[6].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (98 min) demonstrates moderate in vitro antioxidant activity with an ORAC value of 28.8 mmol Trolox/g in the cell-free ORAC assay^[7].
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone (10-100 μM) significantly inhibits adherence of UPEC ATCC®53503TM to T24 bladder epithelial cells at 100 μM, with an inhibition rate of 19.4%, and shows no cytotoxicity at concentrations up to 100 μM^[8].

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