[1]. Chen W, et al. Camphor–a fumigant during the Black Death and a coveted fragrant wood in ancient Egypt and Babylon–a review. Molecules. 2013 May 10;18(5):5434-54.
Alantolactone is a selective STAT3 inhibitor, with potent anticancer activity. Alantolactone induces apoptosis in cancer[1][2][3].
IC50 & Target
STAT3
体外研究 (In Vitro)
Alantolactone induces apoptosis in HepG2 cells in a dose-dependent manner. This Alantolactone-induced apoptosis is found to be associated with GSH depletion, inhibition of STAT3 activation, ROS generation, mitochondrial transmembrane potential dissipation, and increased Bax/Bcl-2 ratio and caspase-3 activation[1]. Alantolactone decreases STAT3 translocation to the nucleus, its DNA-binding, and STAT3 target gene expression. Alantolactone significantly inhibits STAT3 activation with a marginal effect on MAPKs and on NF-κB transcription; however, this effect is not mediated by inhibiting STAT3 upstream kinases[2]. Alantolactone induces activin/SMAD3 signaling in human colon adenocarcinoma HCT-8 cells. Alantolactone performs its antitumor effect by interrupting the interaction between Cripto-1 and the activin receptor type IIA in the activin signaling pathway[4]. Alantolactone (5 μg/mL, 24 h) inhibits cell proliferation in colon adenocarcinoma HCT-8 cells[4].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[4]
Cell Line:
HCT-8 cells.
Concentration:
5 μg/mL (~21.6 μM).
Incubation Time:
24 h.
Result:
Activated the activin signaling pathway in HCT-8 cells.
体内研究 (In Vivo)
It is found that the average tumor volume in the Alantolactone-treated mice is approximately 2.17-fold lower compared with that in the control mice. However the administration of Alantolactone does not affect the overall bodyweight during the experimental period, suggesting no apparent toxicity. Additionally, the average tumor weight is significantly lower in the Alantolactone-treated mice compared with the control mice. What’s more, the administration of Alantolactone results in a significant decrease in p-STAT3 and cyclin D1 expression in the tumor tissues[2].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Female athymic BALB/c nude mice at the age of 6 weeks[2].
Dosage:
2.5 mg/kg.
Administration:
I.P. injection every 2 days.
Result:
Exhibited anti-cancer activity.
分子量
232.32
Formula
C15H20O2
CAS 号
546-43-0
中文名称
土木香内酯;木香腦;土木香脑;阿兰内酯;木香油內酯
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Khan M, et al. Alantolactone induces apoptosis in HepG2 cells through GSH depletion, inhibition of STAT3 activation, and mitochondrial dysfunction. Biomed Res Int. 2013;2013:719858.
[2]. Chun J, et al. Alantolactone selectively suppresses STAT3 activation and exhibits potent anticancer activity in MDA-MB-231 cells. Cancer Lett. 2015 Feb 1;357(1):393-403.
Camphor ((±)-Camphor) is a topical anti-infective and anti-pruritic and internally as a stimulant and carminative. However, Camphor is poisonous when ingested. Antiviral, antitussive, and anticancer activities[1]. Camphor is a TRPV3 agonist[2].
IC50 & Target
TRPV3[2]
体外研究 (In Vitro)
Camphor induces fibroblast proliferation through the PI3K/AKT and ERK signaling pathways[3]. The MTT assay results show that 32.5, 65, 130, and 260 μM Camphor increase fibroblast viability to 108.9±6.6%, 118.6±2.8%, 127.7±4.2%, and 131.6±7.2%, respectively, compared to 0 μM Camphor treatment[3]. Camphor (0-260 μM) treatment for 24 hours increases the generation of ROS by up to 17.97% compared to 5.04% in the no-treatment control[3]. Camphor (0-260 μM, 24 hours) induces the phosphorylation of PI3K, AKT, ERK, and 4EBP1 in a dose- and time-dependent manner[3].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[3]
Cell Line:
Primary dermal fibroblast cells
Concentration:
0-260 μM
Incubation Time:
24 hours
Result:
32.5, 65, 130, and 260 μM increased fibroblast viability to 108.9±6.6%, 118.6±2.8%, 127.7±4.2%, and 131.6±7.2%, respectively, compared to 0 μM treatment.
Western Blot Analysis[3]
Cell Line:
Primary dermal fibroblast cells
Concentration:
0-260 μM
Incubation Time:
24 hours
Result:
Induced the phosphorylation of PI3K, AKT, ERK, and 4EBP1, a repressor of mRNA translation and mTOR substrate, in a dose- and time-dependent manner.
Clinical Trial
分子量
152.23
Formula
C10H16O
CAS 号
76-22-2
中文名称
樟脑
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Chen W, et al. Camphor–a fumigant during the Black Death and a coveted fragrant wood in ancient Egypt and Babylon–a review. Molecules. 2013 May 10;18(5):5434-54.
[2]. Billen B, et al. Different ligands of the TRPV3 cation channel cause distinct conformational changes as revealedby intrinsic tryptophan fluorescence quenching. J Biol Chem. 2015 May 15;290(20):12964-74.
[3]. Tran TA, et al. Camphor Induces Proliferative and Anti-senescence Activities in Human Primary Dermal Fibroblasts and Inhibits UV-Induced Wrinkle Formation in Mouse Skin. Phytother Res. 2015 Dec;29(12):1917-25.