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Lactucin
Lactucin
ChemFaces products have been cited in many studies from excellent and top scientific journals
Product Name Lactucin
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CAS No.: 1891-29-8
Catalog No.: CFN91605
Molecular Formula: C15H16O5
Molecular Weight: 276.28 g/mol
Purity: >=98%
Type of Compound: Sesquiterpenoids
Physical Desc.: Powder
Source: The herbs of Lactuca virosa
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Download: COA    MSDS
Similar structural: Comparison
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Related Screening Libraries
Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
10 mM * 1 mL in DMSO / Inquiry / In-stock
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Biological Activity
Description: Lactucin exerting anti-malaria and anti-hyperalgesia, anti-adipogenesis and anti-inflammatory effects. Lactucin is an anti-inflammatory agent. Lactucin induces cancer cell apoptosis. Lactucin also shows analgesic, anticancer and antimalarial activities.
In vitro:
Genes Genomics . 2021 Oct;43(10):1199-1207.
Lactucin induces apoptosis through reactive oxygen species-mediated BCL-2 and CFLAR L downregulation in Caki-1 cells[Pubmed: 34302634]
Background: Lactucin, a naturally occurring active sesquiterpene lactone, is abundantly found in chicory and romaine lettuce. A recent study reported that Lactucin could induce apoptosis in leukemia cells. However, its cytotoxicity and potential molecular mechanisms underlying cancer cell death remain unclear. Objective: Therefore, in this study, we aimed to investigate the direct effect and underlying mechanism of action of Lactucin on renal cancer cells. Methods: MTT assay and flow cytometry were performed to evaluate the rate of cell proliferation and apoptosis, respectively. Western blotting, reverse transcription polymerase chain reaction, and protein stability analyses were performed to analyze the effect of Lactucin on the expression of apoptosis-related proteins such as B-cell lymphoma 2 (BCL-2) and CFLAR (CASP8 and FADD like apoptosis regulator) long isoform (CFLARL) in Caki-1 human renal cancer cells. In addition, reactive oxygen species (ROS) generation was evaluated using flow cytometry. Results: Lactucin treatment induced apoptosis in Caki-1 cells in a dose-dependent manner via activation of the caspase pathway. It downregulated BCL-2 and CFLARL expression levels by suppressing BCL-2 transcription and CFLARL protein stability, respectively. Pretreatment with N-acetyl-1-cysteine, a ROS scavenger, attenuated the Lactucin-induced apoptosis and restored the BCL-2 and CFLARL expression to basal levels. Lactucin-facilitated BCL-2 downregulation was regulated at the transcriptional level through the inactivation of the NF-κB pathway. Conclusions: Our study is the first to demonstrate that Lactucin-induced apoptosis is mediated by ROS production, which in turn activates the caspase-dependent apoptotic pathway by inhibiting BCL-2 and CFLARL expression in Caki-1 cells.
Cells . 2020 Jan 31;9(2):331.
A Potential Nutraceutical Candidate Lactucin Inhibits Adipogenesis through Downregulation of JAK2/STAT3 Signaling Pathway-Mediated Mitotic Clonal Expansion[Pubmed: 32023857]
The prevalence of obesity has increased dramatically worldwide in the past ~50 years. Searching for safe and effective anti-obesity strategies are urgently needed. Lactucin, a plant-derived natural small molecule, is known for anti-malaria and anti-hyperalgesia. The study is to investigate whether Lactucin plays a key role in adipogenesis. To this end, in vivo male C57BL/6 mice fed a high-fat diet (HFD) were treated with 20 mg/kg/day of Lactucin or vehicle by gavage for seven weeks. Compared with vehicle-treated controls, Lactucin-treated mice showed lower body mass and mass of adipose tissue. Consistently, in vitro 3T3-L1 cells were treated with 20 μM of Lactucin. Compared to controls, Lactucin-treated cells showed significantly less lipid accumulation during adipocyte differentiation and lower levels of lipid synthesis markers. Mechanistically, we showed the anti-adipogenic property of Lactucin was largely limited to the early stage of adipogenesis. Lactucin-treated cells fail to undergo mitotic clonal expansion (MCE). Further studies demonstrate that Lactucin-induced MCE arrests might result from reduced phosphorylation of JAK2 and STAT3. We then asked whether activation of JAK2/STAT3 would restore the inhibitory effect of Lactucin on adipogenesis with pharmacological STAT3 activator colivelin. Our results revealed similar levels of lipid accumulation between Lactucin-treated cells and controls in the presence of colivelin, indicating that inactivation of STAT3 is the limiting factor for the anti-adipogenesis of Lactucin in these cells. Together, our results provide the indication that Lactucin exerts an anti-adipogenesis effect, which may open new therapeutic options for obesity.
In vivo:
Cells . 2020 Jan 31;9(2):331.
A Potential Nutraceutical Candidate Lactucin Inhibits Adipogenesis through Downregulation of JAK2/STAT3 Signaling Pathway-Mediated Mitotic Clonal Expansion[Pubmed: 32023857]
The prevalence of obesity has increased dramatically worldwide in the past ~50 years. Searching for safe and effective anti-obesity strategies are urgently needed. Lactucin, a plant-derived natural small molecule, is known for anti-malaria and anti-hyperalgesia. The study is to investigate whether Lactucin plays a key role in adipogenesis. To this end, in vivo male C57BL/6 mice fed a high-fat diet (HFD) were treated with 20 mg/kg/day of Lactucin or vehicle by gavage for seven weeks. Compared with vehicle-treated controls, Lactucin-treated mice showed lower body mass and mass of adipose tissue. Consistently, in vitro 3T3-L1 cells were treated with 20 μM of Lactucin. Compared to controls, Lactucin-treated cells showed significantly less lipid accumulation during adipocyte differentiation and lower levels of lipid synthesis markers. Mechanistically, we showed the anti-adipogenic property of Lactucin was largely limited to the early stage of adipogenesis. Lactucin-treated cells fail to undergo mitotic clonal expansion (MCE). Further studies demonstrate that Lactucin-induced MCE arrests might result from reduced phosphorylation of JAK2 and STAT3. We then asked whether activation of JAK2/STAT3 would restore the inhibitory effect of Lactucin on adipogenesis with pharmacological STAT3 activator colivelin. Our results revealed similar levels of lipid accumulation between Lactucin-treated cells and controls in the presence of colivelin, indicating that inactivation of STAT3 is the limiting factor for the anti-adipogenesis of Lactucin in these cells. Together, our results provide the indication that Lactucin exerts an anti-adipogenesis effect, which may open new therapeutic options for obesity.
J Ethnopharmacol . 2006 Sep 19;107(2):254-258.
Analgesic and sedative activities of lactucin and some lactucin-like guaianolides in mice[Pubmed: 16621374]
Lactucin (1) and its derivatives lactucopicrin (2) and 11beta,13-dihydroLactucin (3), which are characteristic bitter sesquiterpene lactones of Lactuca virosa and Cichorium intybus, were evaluated for analgesic and sedative properties in mice. The compounds showed analgesic effects at doses of 15 and 30 mg/kg in the hot plate test similar to that of ibuprofen, used as a standard drug, at a dose of 30 mg/kg. The analgesic activities of the compounds at a dose of 30 mg/kg in the tail-flick test were comparable to that of ibuprofen given at a dose of 60 mg/kg. Lactucopicrin appeared to be the most potent analgetic of the three tested compounds. Lactucin and lactucopicrin, but not 11beta,13-dihydroLactucin, also showed sedative properties in the spontaneous locomotor activity test.
Front Pharmacol . 2021 Apr 29;12:683613.
Cichorium pumilum Jacq Extract Inhibits LPS-Induced Inflammation via MAPK Signaling Pathway and Protects Rats From Hepatic Fibrosis Caused by Abnormalities in the Gut-Liver Axis[Pubmed: 33995112]
The development of liver fibrosis is closely related to the gut microbiota, and the "gut-liver axis" is the most important connection between the two. ethyl acetate extract of Cichorium pumilum Jacq (CGEA) is an herbal extract consisting mainly of sesquiterpenoids. The anti-inflammatory and hepatoprotective effects of CGEA have been reported, but the anti-fibrotic effects of CGEA via intestinal microbes and the "gut-liver axis" cycle have rarely been reported. In this study, we observed that CGEA not only directly attenuated inflammatory factor levels in inflamed mice, but also attenuated liver inflammation as well as liver fibrosis degeneration in rats with liver fibrosis caused by colitis. We observed in vitro that CGEA significantly promoted the growth of Bifidobacterium adolescentis. Similarly, fecal 16S rDNA sequencing of liver fibrosis rats showed that CGEA intervention significantly altered the composition of the intestinal microbiota of liver fibrosis rats. CGEA increased the abundance of intestinal microbiota, specifically, CGEA increased the ratio of Firmicutes to Bacteroidetes, CGEA could significantly increase the levels of Ruminococcus. In addition, CGEA intervention significantly protected intestinal mucosal tissues and improved intestinal barrier function in rats. Lactucin is the main sesquiterpenoid in CGEA, and HPLC results showed its content in CGEA was up to 6%. Lactucin has been reported to have significant anti-inflammatory activity, and in this study, we found that Lactucin decreased p38 kinases (p38), phosphorylation of the extracellular signal-regulated kinase (ERK) and protein kinase B (AKT) protein phosphorylation in lipopolysaccharide (LPS)-activated RAW264.7 cells, thereby reducing mRNA expression and protein expression of pro-inflammatory factors inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), and inhibiting the release of inflammatory factors interleukin (IL)-6 and nitric oxide (NO), exerting anti-inflammatory effects. In summary, the prevention of liver fibrosis caused by intestinal inflammation by CGEA may be achieved by regulating the intestinal microbiota and restoring the intestinal barrier thereby improving the "gut-liver axis" circulation, reducing liver inflammation, and ultimately alleviating liver fibrosis. Notably, the direct anti-inflammatory effect of CGEA may be due to its content of Lactucin, which can exert anti-inflammatory effects by inhibiting the phosphorylation of Mitogen-activated protein kinase (MAPK) and Akt signaling pathways.
Evid Based Complement Alternat Med . 2018 Oct 18;2018:8549519.
Preparation of Magnetic Nanoliposomes of Sesquiterpene-Rich Fraction from Cichorium glandulosum and Its Tissue Distribution in Mice[Pubmed: 30420898]
Objective: To prepare and study the distribution of magnetic nanoliposomes of Sesquiterpene-Rich Fraction from Cichorium glandulosum (SRF-MLN) (under magnetic field) in the main organs of mice. Methods: The SRF-MLN was prepared by ethanol injection-sonication precipitation method. The quality of its pharmaceutical properties was investigated by the active ingredient Lactucin. The drug concentration and distribution of Lactucin in different tissues and organs including whole blood, liver, heart, spleen, lung, and kidney were evaluated with Sesquiterpene-Rich Fraction from Cichorium glandulosum (SRF-LP) as a control. Results: The prepared SRF-MLN was spherical and monodispersed with an average particle diameter of 65 ± 1 nm, encapsulation efficiency of 91.3% ± 1.5% (RSD% = 1.5), and drug loading rate of 4.7% ± 0.3% (RSD% = 0.7). Dispersion coefficient PDI was 0.157 and Zeta potential was -17.5 mV. The Lactucin concentration of SRF-MLN after 10 min of intravenous injection in heart, liver, spleen, lung, and kidney was significantly higher than that of SRF-LP group. The AUC0-12h values of liver tissue were obviously higher than other tissues and MRT was significantly prolonged under the action of the magnetic field (p<0.01). Conclusion: The prepared SRF-MLN can change the distribution of drugs in different tissues and organs, prolonging the action time of the drugs in the body, and it has certain specificity under the action of applied magnetic field.
Lactucin Description
Source: The herbs of Lactuca virosa
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Calculate Dilution Ratios(Only for Reference)
1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.6195 mL 18.0976 mL 36.1952 mL 72.3903 mL 90.4879 mL
5 mM 0.7239 mL 3.6195 mL 7.239 mL 14.4781 mL 18.0976 mL
10 mM 0.362 mL 1.8098 mL 3.6195 mL 7.239 mL 9.0488 mL
50 mM 0.0724 mL 0.362 mL 0.7239 mL 1.4478 mL 1.8098 mL
100 mM 0.0362 mL 0.181 mL 0.362 mL 0.7239 mL 0.9049 mL
* Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
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