a-Bitter Acid/(R)-3,5,6-Trihydroxy-2-isovaleryl-4,6-bis-(3-methyl-but-2-enyl)-cyclohexa-2,4-dienon/2,4-Cyclohexadien-1-one, 3,5,6-trihydroxy-2-isovaleryl-4,6-bis(3-methyl-2-butenyl)-, (R)-(-)-/3,5,6β-Trihydroxy-2-isovaleryl-4,6α-bis(3-methyl-2-butenyl)-2,4-cyclohexadienon/Humulon/(6R)-3,5,6-trihydroxy-2-isovaleryl-4,6-bis(3-methylbut-2-enyl)cyclohexa-2,4-dienone/a-Lupulic Acid/2,4-Cyclohexadien-1-one, 3,5,6-trihydroxy-4,6-bis(3-methyl-2-buten-1-yl)-2-(3-methyl-1-oxobutyl)-, (6R)-/2,4-Cyclohexadien-1-one, 3,5,6-trihydroxy-4,6-bis(3-methyl-2-butenyl)-2-(3-methyl-1-oxobutyl)-, (R)-/(R)-2.3.6-Trihydroxy-1.3-bis-(3-methyl-buten-(2)-yl)-5-isovaleryl-cyclohexadien-(1.5)-on-(4)/α-Lupulic acid/(R)-3,5,6-trihydroxy-2-isovaleryl-4,6-bis-(3-methyl-but-2-enyl)-cyclohexa-2,4-dienone/(6R)-3,5,6-Trihydroxy-2-(3-methylbutanoyl)-4,6-bis(3-methyl-2-buten-1-yl)-2,4-cyclohexadien-1-one/Humulone,mixture of homologues/|A-Lupulic acid/2',3'-Dihydro-3'β,4',6'-trihydroxy-3'α,5'-bis(3-methyl-2-butenyl)-2'-oxoisovalerophenon/(R)-3,5,6-Trihydroxy-4,6-bis(3-methyl-2-butenyl)-2-(3-methyl-1-oxobutyl)-2,4-cyclohexadien-1-one/(6R)-3,5,6-Trihydroxy-2-(3-methylbutanoyl)-4,6-bis(3-methylbut-2-en-1-yl)cyclohexa-2,4-dien-1-one/|A-Bitter acid/Humulone/humulone, (R)-/α-Bitter acid
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
571.4±50.0 °C at 760 mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:26472-41-3) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Respiratory syncytial virus (RSV) is the major infectious agent causing serious respiratory tract inflammation in infants and young children. However, an effective vaccine and anti-viral therapy for RSV infection have not yet been developed. Hop-derived bitter acids have potent pharmacological effects on inflammation. Therefore, we investigated the effects of humulone, which is the main constituent of hop bitter acids, on the replication of RSV and release of the proinflammatory cytokine IL-8 and chemokine RANTES in RSV-infected human nasal epithelial cells (HNECs). We found that humulone prevented the expression of RSV/G-protein, formation of virus filaments and release of IL-8 and RANTES in a dose-dependent manner in RSV-infected HNECs. These findings suggest that humulone has protective effects against the replication of RSV, the virus assembly and the inflammatory responses in HNECs and that it is a useful biological product for the prevention and therapy for RSV infection.
Humulone suppresses replication of respiratory syncytial virus and release of IL-8 and RANTES in normal human nasal epithelial cells.
Fuchimoto J1, Kojima T, Okabayashi T, Masaki T, Ogasawara N, Obata K, Nomura K, Hirakawa S, Kobayashi N, Shigyo T, Yokota S, Fujii N, Tsutsumi H, Himi T, Sawada N.
2013 Dec 9
Humulone, a bitter acid derived from hop (Humulus lupulus L.), possesses antioxidative, anti-inflammatory and other biologically active activities. Although humulone has been reported to inhibit chemically induced mouse skin tumor promotion, the underlying mechanisms are yet to be elucidated. Since an inappropriate over-expression of cyclooxygenase-2 (COX-2) is implicated in carcinogenesis, we investigated effects of humulone on COX-2 expression in mouse skin stimulated with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA). Topical application of humulone (10 mumol) significantly inhibited TPA-induced epidermal COX-2 expression. Humulone also diminished TPA-induced DNA binding of nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1). Pre-treatment with humulone attenuated TPA-induced phosphorylation of p65 and nuclear translocation of NF-kappaB subunit proteins. Humulone blunted TPA-induced activation of inhibitory kappaB (IkappaB) kinase (IKK) in mouse skin, which accounts for its suppression of phosphorylation and subsequent degradation of IkappaBalpha. An in vitro kinase assay revealed that humulone could directly inhibit the catalytic activity of IKKbeta. Humulone suppressed the activation of mitogen-activated protein kinases (MAPKs) in TPA-treated mouse skin. The roles of extracellular signal-regulated protein kinase-1/2 and p38 MAPK in TPA-induced activation of NF-kappaB in mouse skin had been defined in our previous studies. The present study revealed that topical application of SP600125, a pharmacological inhibitor of c-Jun-N-terminal kinase (JNK), abrogated the activation of AP-1 and the expression of COX-2 in TPA-treated mouse skin. Taken together, humulone suppressed TPA-induced activation of NF-kappaB and AP-1 and subsequent expression of COX-2 by blocking upstream kinases IKK and JNK, respectively, which may account for its antitumor-promoting effects on mouse skin carcinogenesis.
Humulone inhibits phorbol ester-induced COX-2 expression in mouse skin by blocking activation of NF-kappaB and AP-1: IkappaB kinase and c-Jun-N-terminal kinase as respective potential upstream targets.
Lee JC1, Kundu JK, Hwang DM, Na HK, Surh YJ.
Humulone, a bone resorption inhibitor isolated from hop extract, induced apoptosis in the premyocytic leukemia cell line HL-60 between 1 and 100 micrograms/ml. Our data suggested that there was a correlation between the apoptosis-inducing activity of humulone and its antioxidative activity.
Apoptosis to HL-60 by humulone.
Tobe H1, Kubota M, Yamaguchi M, Kocha T, Aoyagi T.