White crystalline powder
(3b,5a,22b,25S)-Spirosolan-3-ol/(3β,5α,22β,25S)-spirosolan-3-ol/Spirosolan-3-ol, (3β,5α,22β,25S)- (9CI)/5alpha-Tomatidan-3beta-ol/(22S,25S)-5α-spirosolan-3β-ol/(2S,4aS,4bS,5'S,6aS,6bR,7S,8S,9aS,10aS,10bR,12aS)-4a,5',6a,7-Tetramethyloctadecahydrospiro[naphtho[2',1':4,5]indeno[2,1-b]furan-8,2'-piperidin]-2-ol/(2S,4aS,4bS,5'S,6aS,6bR,7S,8S,9aS,10aS,10bR,12aS)-4a,5',6a,7-Tetramethyloctadecahydrospiro[naphto[2',1':4,5]indeno[2,1-b]furane-8,2'-piperidin]-2-ol/5a,20bF,22aF,25bF,27-azaspirostan-3b-ol/(3β,5α,25S)-Spirosolan-3-ol/Tomatidine/Spirosolan-3-ol, (3β,5α,25S)-/Tomatidin
527.2±25.0 °C at 760 mmHg
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provides coniferyl ferulate(CAS#:77-59-8) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Aging is a major international concern that brings formidable socioeconomic and healthcare challenges. Small molecules capable of improving the health of older individuals are being explored. Small molecules that enhance cellular stress resistance are a promising avenue to alleviate declines seen in human aging. Tomatidine, a natural compound abundant in unripe tomatoes, inhibits age-related skeletal muscle atrophy in mice. Here we show that tomatidine extends lifespan and healthspan in C. elegans, an animal model of aging which shares many major longevity pathways with mammals. Tomatidine improves many C. elegans behaviors related to healthspan and muscle health, including increased pharyngeal pumping, swimming movement, and reduced percentage of severely damaged muscle cells. Microarray, imaging, and behavioral analyses reveal that tomatidine maintains mitochondrial homeostasis by modulating mitochondrial biogenesis and PINK-1/DCT-1-dependent mitophagy. Mechanistically, tomatidine induces mitochondrial hormesis by mildly inducing ROS production, which in turn activates the SKN-1/Nrf2 pathway and possibly other cellular antioxidant response pathways, followed by increased mitophagy. This mechanism occurs in C. elegans, primary rat neurons, and human cells. Our data suggest that tomatidine may delay some physiological aspects of aging, and points to new approaches for pharmacological interventions for diseases of aging.
Tomatidine enhances lifespan and healthspan in C. elegans through mitophagy induction via the SKN-1/Nrf2 pathway.
Fang EF1, Waltz TB1, Kassahun H1,2, Lu Q1, Kerr JS1, Morevati M1,3, Fivenson EM1, Wollman BN1, Marosi K4, Wilson MA4, Iser WB4, Eckley DM5, Zhang Y5, Lehrmann E5, Goldberg IG5, Scheibye-Knudsen M1,3, Mattson MP4, Nilsen H2, Bohr VA1,3, Becker KG5.
2017 Apr 11
Despite of the most effective surgical removal of malignant tumors, metastasis makes cancer treatment difficult. The studies on natural compounds to inhibit this metastasis have been actively performed until now. However, the effect of tomatidine on metastasis remains unclear.
The effect of tomatidine on antioxidative activity was measured with DPPH radical assay and reducing power assay. After treatment with tomatidine, the viability of human fibrosarcoma cells (HT1080 cells) was evaluated with MTT assay. The effect of tomatidine on the inhibition of matrix metalloproteinase-2 (MMP-2) and MMP-9, gelatinases related to metastasis, was analyzed using gelatin zymography, western blot and immunofluorescence staining. Cell invasion assay was used to investigate anti-metastasis activity of tomatidine.
Tomatidine showed no DPPH radical scavenging effect and showed 8% of reduction power at 8 μM. Furthermore, tomatidine below 8 μM showed more than 80% of cell viability in MTT assay. The inhibition of tomatidine on MMP-2 activity and its protein expression levels were observed by gelatin zymography, western blot and immunofluorescence. It was observed that tomatidine inhibited not only p38 and ERK but also cell invasion.
Above results suggest that tomatidine could use as a potential candidate for cancer prevention and metastasis through the inhibitory effect on gelatinase.
Copyright © 2019 Elsevier B.V. All rights reserved.
AP-1; ERK; Gelatinase; Metastasis; Tomatidine; p38
Tomatidine inhibits cell invasion through the negative modulation of gelatinase and inactivation of p38 and ERK.
Jeon S1, Kim MM2.
2019 Nov 1
Dengue is the most common arboviral disease worldwide with 96 million symptomatic cases annually. Despite its major impact on global human health and huge economic burden there is no antiviral drug available to treat the disease. The first tetravalent dengue virus vaccine was licensed in 2015 for individuals aged 9 to 45, however, most cases are reported in infants and young children. This, together with the limited efficacy of the vaccine to dengue virus (DENV) serotype 2, stresses the need to continue the search for compounds with antiviral activity to DENV. In this report, we describe tomatidine as a novel compound with potent antiviral properties towards all DENV serotypes and the related Zika virus. The strongest effect was observed for DENV-2 with an EC50 and EC90 value of 0.82 and 1.61 μM, respectively, following infection of Huh7 cells at multiplicity of infection of 1. The selectivity index is 97.7. Time-of-drug-addition experiments revealed that tomatidine inhibits virus particle production when added pre, during and up to 12 h post-infection. Subsequent experiments show that tomatidine predominantly acts at a step after virus-cell binding and membrane fusion but prior to the secretion of progeny virions. Tomatidine was found to control the expression of the cellular protein activating transcription factor 4 (ATF4), yet, this protein is not solely responsible for the observed antiviral effect. Here, we propose tomatidine as a candidate for the treatment of dengue given its potent antiviral activity.
Copyright © 2018 Elsevier B.V. All rights reserved.
Activating transcription factor 4; Antiviral; Dengue virus; Tomatidine
Tomatidine, a novel antiviral compound towards dengue virus.
Diosa-Toro M1, Troost B2, van de Pol D2, Heberle AM3, Urcuqui-Inchima S4, Thedieck K5, Smit JM6.
Tomatidine acts as an anti-inflammatory agent by blocking NF-κB and JNK signaling.