2-Undecanone

2-Undecanone is an orally active organic ketone. 2-Undecanone exerts antibacterial effects by inhibiting bacterial chaperone systems and interfering with the refolding of heat-inactivated proteins. 2-Undecanone also ameliorates asthmatic inflammation and airway remodeling by blocking the NF-κB pathway, and activates the Nrf2 pathway to reduce oxidative damage and prevent lung cancer induced by Benzo[a]pyrene (HY-107377). 2-Undecanone can be used in research related to cancer, asthma and infections^[1][2][3]. In Vitro:2-Undecanone (6.25-200 μM; 48 h) exhibits low intrinsic cytotoxicity toward BEAS-2B cells, and reverses Benzo[a]pyrene (B[a]P) (HY-107377)-induced cytotoxicity in a dose-dependent manner^[1].
2-Undecanone (25-100 μM; 48 h) dose-dependently reverses B[a]P-induced G0/G1 cell cycle arrest in BEAS-2B cells and restores the expression of cyclin D1^[1].
2-Undecanone (25-100 μM; 48 h) reduces B[a]P-induced DNA strand breaks in BEAS-2B cells^[1].
2-Undecanone (25-100 μM; 48 h) dose-dependently reduces B[a]P-induced overexpression of p-H2A.X in BEAS-2B cells, indicating that it can alleviate DNA double-strand breaks^[1].
2-Undecanone (25-100 μM; 24 h) dose-dependently reduces B[a]P-induced overexpression of IL-1β and pro-IL-1β in BEAS-2B cells, indicating that it inhibits inflammatory responses^[1].
2-Undecanone (25-100 μM; 48 h) reduces the excessive intracellular ROS production induced by B[a]P in BEAS-2B cells^[1].
2-Undecanone (50 μM) activates the Nrf2-HO-1/NQO-1 signaling pathway in BEAS-2B cells and reverses the inhibitory effect of B[a]P on this pathway in BEAS-2B cells^[1].
2-Undecanone (50 μM; 24-48 h) exerts protective effects against B[a]P-induced cytotoxicity, excessive ROS production and DNA damage in BEAS-2B cells via the Nrf2-HO-1/NQO-1 signaling pathway^[1].
2-Undecanone (20 μmol; 0-90 min) almost completely inhibits the DnaK-ClpB-dependent refolding of heat-inactivated Photobacterium leiognathi luciferase in cell lysates of Escherichia coli JW3663 ibpB::kan (pLeo1)^[2].
2-Undecanone (12.5-50 μM; 48 h) inhibits PDGF-BB-induced proliferation of primary mouse airway smooth muscle cells in a dose-dependent manner when co-incubated with 20 ng/mL PDGF-BB^[3].
2-Undecanone (12.5-50 μM; 48 h) dose-dependently attenuates PDGF-BB-induced migration of primary mouse airway smooth muscle cells pretreated with 20 ng/mL PDGF-BB^[3].
When co-incubated with 20 ng/mL PDGF-BB, 2-Undecanone (12.5-50 μM; 48 h) dose-dependently reverses PDGF-BB-induced phenotypic switch of primary mouse airway smooth muscle cells from the contractile to the synthetic phenotype, restores calmodulin expression and reduces osteopontin expression^[3].
2-Undecanone (12.5-50 μM; 48 h) inhibits PDGF-BB-induced secretion of the proinflammatory cytokines IL-6 and TNF-α from primary mouse airway smooth muscle cells in a dose-dependent manner^[3].
2-Undecanone (50 μM; 48 h) inhibits PDGF-BB-induced activation of the NF-κB pathway in primary mouse airway smooth muscle cells during co-incubation with 20 ng/mL PDGF-BB, reduces the phosphorylation levels of IκBα and NF-κB p65, and blocks the nuclear translocation of NF-κB p65^[3]. In Vivo:2-Undecanone (100-200 mg/kg; p.o.; five times weekly; 38 weeks) significantly inhibits B[a]P-induced lung tumorigenesis in A/J mice with tumor inhibition rates of 33.62 ± 14.60% and 38.26 ± 13.59%, respectively, while also reducing DNA damage and systemic inflammation^[1].
2-Undecanone (100-400 mg/kg; i.g.; once daily; 7 days) dose-dependently alleviates OVA-induced asthma in female BALB/c mice by reducing airway inflammation, histopathological lung changes, and activation of the NF-κB pathway^[3].