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  • Brand : BIOFRON

  • Catalogue Number : BF-C3019

  • Specification : 98%

  • CAS number : 2415-24-9

  • Formula : C15H22O10

  • Molecular Weight : 362.33

  • PUBCHEM ID : 91520

  • Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

Rehmannia glutinosa

Structure Type



Standards;Natural Pytochemical;API




catalpinoside/des-p-hydroxybenzoyl-catalposid/CATAPOL/6-Hydroxy-1a-(hydroxymethyl)-1a,1b,2,5a,6,6a-hexahydrooxireno[4,5]cyclopenta[1,2-c]pyran-2-yl hexopyranoside/Hexopyranoside, 1a,1b,2,5a,6,6a-hexahydro-6-hydroxy-1a-(hydroxymethyl)oxireno[4,5]cyclopenta[1,2-c]pyran-2-yl/catalposide/methyl iridoid glycoside




1.7±0.1 g/cm3


Methanol; Ethanol; DMSO

Flash Point

362.4±31.5 °C

Boiling Point

675.6±55.0 °C at 760 mmHg

Melting Point



InChl Key

WGK Germany


HS Code Reference


Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:2415-24-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Catalpol, an iridoid glucoside compound, is reported to possess diverse pharmacological actions. However, its effects on osteosarcoma are little to be known. In the present study, we showed that catalpol could strongly suppress osteosarcoma progression. Catalpol dose-dependently reduced the cancer cell viability. The migration of osteosarcoma cells was also consistently suppressed by catalpol treatment using the wound healing and transwell migration analysis. Catalpol reduced the expressions of Kras, receptor for activated C-kinase 1(RACK1) and matrix metalloproteinase (MMP)-2 in a dose-dependent manner, revealing the blockage of migration. Moreover, both intrinsic and extrinsic apoptosis were triggered by catalpol, as evidenced by improved cleaved Caspase-8/-9/-3 and Poly-(ADP-ribose) polymerase (PARP). Release of Cyto-c in cytoplasm and Bax up-regulation in total cells were observed in catalpol-treated cells, while mitochondrial Cyto-c and cellular Bcl-2 were down-regulated by catalpol. Reactive oxygen species (ROS) production was also involved in catalpol-induced cell death. Further, ROS scavenger, N-acetylcysteine (NAC), impeded catalpol-caused apoptosis. And suppression of signal transducer and activator of transcription 3/Janus kinase 2 gene/Src (STAT3/JAK2/Src) was involved in catalpol-induced cell death. In vivo, catalpol showed effective ability to reduce the tumor growth. Our results illustrated that catalpol might be considered as a promising pharmacological agent to suppress osteosarcoma.


Apoptosis and ROS; Catalpol; Migration; Osteosarcoma; STAT3/JAK2.


Catalpol Suppresses Osteosarcoma Cell Proliferation Through Blocking Epithelial-Mesenchymal Transition (EMT) and Inducing Apoptosis


Lei Wang 1 , Gui-Bin Xue 2

Publish date

2018 Jan 1




Tumor angiogenesis and inflammation, which play important roles in mediating tumor proliferation and growth, should be inhibited to effectively regulate tumor progression. Catalpol, a main active ingredient extracted from Rehmannia glutinosa, has various pharmacological actions including anti-apoptotic, anti-inflammatory, hypoglycemic and anti-cancer properties. However, the pharmacological effect of catalpol on colon cancer remains largely unknown. The aim of this study was to investigate the effects of catalpol on the proliferation, growth, invasion, tumor angiogenesis and inflammation of CT26 colon cancer in vitro and in vivo. Catalpol inhibited the proliferation and growth of CT26 cells in concentration- and dose-dependent manners in vitro and in vivo, respectively. Catalpol suppressed the invasion of CT26 cells in vitro. Tumor cell-induced vascularization of endothelial cells and rat aortic ring angiogenesis were impaired by catalpol. Catalpol reduced the secretions of several angiogenic markers in the culture supernatant of CT26 cells. Immunohistochemical assay showed that catalpol inhibited the expressions of angiogenic markers vascular endothelial growth factor (VEGF), vascular endothelial growth factor receptor 2 (VEGFR2), hypoxia inducible factor-1α (HIF-1α) and basic fibroblast growth factor (bFGF) in colon cancer tissues. Moreover, catalpol inhibited the expressions of inflammatory factors interleukin-1β (IL-1β), IL-6, IL-8, cyclooxygenase (COX-2) and inducible nitric oxide synthase (iNOS). Taken together, catalpol suppressed the growth and invasion of CT26 colon cancer cells mainly by inhibiting inflammation and tumor angiogenesis, as a promising candidate compound for treating colon cancer.


Apoptosis and ROS; Catalpol; Migration; Osteosarcoma; STAT3/JAK2.


Catalpol Suppressed Proliferation, Growth and Invasion of CT26 Colon Cancer by Inhibiting Inflammation and Tumor Angiogenesis


Pingting Zhu 1 , Yu Wu 2 , Aihua Yang 3 , Xingsheng Fu 4 , Ming Mao 1 , Zhaoguo Liu 5

Publish date

2017 Nov




Type 2 diabetes is characterized by insulin resistance in target tissues and hyperglycemia. Catalpol is a natural product isolated from the root of Rehmannia glutinosa, which has been reported to produce the effect of anti-diabetes in recent reports. The goal of the current study is to investigate the therapeutic effects of catalpol on hepatic insulin resistance in type 2 diabetes and elucidate the underlying cellular mechanisms. Type 2 diabetes in vivo was induced by combined high-fat diet (HFD) and streptozotocin (STZ) injection in C57BL/6J mice. Insulin resistance in vitro was induced by glucosamine administration in HepG2 cells. Catalpol exhibited the effects decreasing hepatic gluconeogenesis and increasing hepatic glycogen synthesis both in vivo and in vitro. Additionally, catalpol improved hepatic NADPH oxidase type 4 (NOX4)-mediated oxidative stress and activated hepatic AMP-activated protein kinase (AMPK) and phosphatidylinositol 3-kinase (PI3K)/AKT pathway in vivo and in vitro. The effects of catalpol on preventing gluconeogenesis and increasing glycogen synthesis in glucosamine-induced HepG2 cells were prevented by pretreatment with LY294002, the inhibitor of PI3K. Furthermore, the effect of catalpol on depriving glucosamine-induced insulin resistance was prevented by knockdown of NOX4 or AMPK with short interfering RNA (siRNA) in HepG2 cells. Moreover, the suppressive effect of catalpol on glucosamine-induced NOX4 over-expression was weakened by knockdown of AMPK with siRNA. Taken together, these findings suggested that catalpol ameliorated hepatic insulin resistance in type 2 diabetes through acting on AMPK/NOX4/PI3K/AKT pathway.


AMPK; Catalpol; Insulin resistance; NOX4; Type 2 diabetes.


Catalpol Ameliorates Hepatic Insulin Resistance in Type 2 Diabetes Through Acting on AMPK/NOX4/PI3K/AKT Pathway


Jiting Yan 1 , Changyuan Wang 1 , Yue Jin 1 , Qiang Meng 1 , Qi Liu 1 , Zhihao Liu 1 , Kexin Liu 1 , Huijun Sun 2

Publish date

2018 Apr

Description :

Catalpol, an iridoid glycoside, has neuroprotective, anti-inflammatory, and anti-hepatitis virus effects.IC50 Value:Target: neuroprotective, anti-inflammatory, and anti-hepatitis virus natural product.In vitro: Catalpol could be encapsulated into composite nanofibers and induce differentiation of hASCs into neural-like cells, which might offer new avenues in nerve regeneration [1].In vivo: The pharmacokinetics of catalpol in normal and doxorubicin-induced chronic kidney disease rats after oral administration of Rehmannia glutinosa extract was determined, and the extraction recoverie of catalpol was higher than 68.24% [2]. The protective effect of catalpol on renal IRI mice through suppressing phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt)-endothelial nitric oxide synthase (eNOS) and against inflammation, and the possible underlying mechanism [3].