Catalogue Number
BF-N2003
Analysis Method
HPLC,NMR,MS
Specification
98%
Storage
2-8°C
Molecular Weight
168.15
Appearance
White crystalline powder
Botanical Source
synthesis
Structure Type
Others
Category
Standards;Natural Pytochemical;API
SMILES
C1CC2C3C(C1O2)C(=O)OC3=O
Synonyms
hexahydro-4,7-epoxyisobenzofuran-1,3-dione/cis-exo-hexahydro-4,7-epoxyisobenzofuran-1,3-dione/7-Oxabicyclo[2.2.1]heptane-2,3-dicarboxylic Anhydride/Demehylcantharidin/Wln: T C555 A ao dvovtj/Hexahydro-3,6-epoxyphthalic anhydride/demethylcantharidin/Nocantharidin/4,7-Epoxyisobenzofuran-1,3-dione, hexahydro-/4,10-Dioxatricyclo[5.2.1.0]decane-3,5-dione/3,6-Endooxyphthalic anhydride,hexahydro
IUPAC Name
4,10-dioxatricyclo[5.2.1.02,6]decane-3,5-dione
Density
1.5±0.1 g/cm3
Solubility
Flash Point
167.0±26.0 °C
Boiling Point
362.5±35.0 °C at 760 mmHg
Melting Point
InChl
InChl Key
WGK Germany
RID/ADR
HS Code Reference
2942000000
Personal Projective Equipment
Correct Usage
For Reference Standard and R&D, Not for Human Use Directly.
Meta Tag
provides coniferyl ferulate(CAS#:5442-12-6) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
COA
31582090
Aiming to enhance therapeutic efficiency and reduce toxic effect of norcantharidin (NCTD), NCTD-conjugated carboxymethyl chitosan (CMCS) conjugates (CNC) were prepared and evaluated for the treatment of hepatocellular carcinoma. In vitro cellular assays revealed that CNC conjugates possessed potent inhibitory effects on the proliferation and migration of BEL-7402 cells. Besides, CNC could change nuclear morphology of tumor cells. In comparison with free NCTD at equivalent dose, CNC exerted enhanced therapeutic efficiency and diminished systemic toxicity in H22 tumor-bearing mice with a tumor inhibition rate of 56.20%. Further investigation about pharmacokinetics and tissue distribution by high performance liquid chromatography (HPLC) analysis indicated that CNC showed a longer retention time in blood circulation and reduced distribution in heart and kidney tissues, thereby exerting different antitumor efficacy and toxicity compared with free NCTD. Our results suggested that CNC conjugates based on CMCS as polymer carriers might be used as a potential clinical alternative for NCTD in tumor therapy.
Copyright © 2019 Elsevier Ltd. All rights reserved.
Carboxymethyl chitosan; Hepatocellular carcinoma; Norcantharidin; Pharmacokinetics; Tissue distribution
Studies on anti-hepatocarcinoma effect, pharmacokinetics and tissue distribution of carboxymethyl chitosan based norcantharidin conjugates.
Chi J1, Jiang Z2, Chen X1, Peng Y2, Liu W1, Han B3, Han B4.
2019 Dec 15
31462369
In this study we employed self-designed PDLLA-PEG-PDLLA (PLEL) thermosensitive hydrogel to blend with norcantharidin (NCTD), a hydrophilic chemotherapeutic drug possessing curative effect on primary hepatocellular carcinoma (HCC) and adverse effects, then utilized the composite in HCC interstitial chemotherapy. PLEL copolymer was synthesized by ring-opening polymerization, NCTD-loaded PLEL hydrogel was prepared in a simple and reasonable way. The addition of NCTD had no significant effect on the temperature-dependent rheological properties of PLEL hydrogel. The pH values of NCTD-loaded gel solutions (13 wt%) and free NCTD solutions with three drug concentrations of 0.4 mg/mL, 0.8 mg/mL and 1.2 mg/mL under different storage conditions met the pH requirement of small-volume injection. There was no significant difference among the drug release behaviors of NCTD-loaded gels with drug concentrations of 0.4 mg/mL, 0.8 mg/mL and 1.2 mg/mL, they fitted first-order dynamics, exhibited significantly slower drug release than free drug solutions and the release was mainly based on drug diffusion. Drug-loaded gel solution (13 wt%) could evenly distribute throughout tumor tissue before converting into gel after being intratumorally injected and was able to significantly prolong retention time of the drug in tumor compared to free drug solution. The sustained-release performance of NCTD-loaded gel (13 wt%) was confirmed from the perspective of pharmacodynamics in vitro. The in vivo evaluation demonstrated that intratumoral injection of NCTD-loaded PLEL gel (13 wt%) was capable of improving curative effect of the drug and reducing its toxicity.
Intratumoral Injection of Norcantharidin-Loaded Poly(D,L-lactide)-b-Poly(ethylene glycol)-b-Poly(D,L-lactide) Thermosensitive Hydrogel for the Treatment of Primary Hepatocellular Carcinoma.
Xue B, Lei M, Shi K, Wang M, Hao Y, Xiao Y, Yuan L, Peng J, Qian Z.
2019 Oct 1
31315217
Norcantharidin (NCTD), a demethylated analog of cantharidin isolated from blister beetles, has been used as a promising anticancer agent; however, the underlying function of NCTD against human oral squamous cell carcinoma (OSCC) has not been fully understood. Here, this study was aimed to investigate the apoptotic effect and molecular targets of NCTD in human OSCC in vitro and in vivo. The anticancer effects of NCTD and its related molecular mechanisms were evaluated by trypan blue exclusion assay, live/dead assay, western blotting, 4-6-Diamidino-2-Phenylindole (DAPI) staining, flow cytometric analysis, Terminal Deoxynucleotidyl Transferase dUTP Nick end Labeling (TUNEL) assay, and immunohistochemistry. NCTD significantly inhibited cell growth and increased the number of dead cells in HSC-3 and HN22 cell lines. It induced the following apoptotic phenomena: (1) the cleavages of poly (ADP-ribose) polymerase and casepase-3; (2) increase in apoptotic morphological changes (nuclear condensation and fragmentation); (3) increase in annexin V-positive cells or sub-G1 population of cells. NCTD significantly activated the p38 mitogen-activated protein kinase (MAPK) pathway but inactivated the signal transducer and activator of transcription (STAT)3 pathway. A p38 MAPK inhibitor (SB203580) partially attenuated NCTD-induced programmed cell death (apoptosis) in both cell lines, whereas ectopic overexpression of STAT3 did not affect it. NCTD strongly suppressed tumor growth in the tumor xenograft bearing HSC-3 cells, and the number of TUNEL-positive cells increased in NCTD-treated tumor tissues. In addition, NCTD did not cause any histopathological changes in the liver nor the kidney. NCTD induced programmed cell death via the activation of p38 MAPK in OSCC. Therefore, these results suggest that NCTD could be a potential anticancer drug candidate for the treatment of OSCC.
norcantharidin; oral squamous cell carcinoma; p38 MAPK; programmed cell death
Contribution of p38 MAPK Pathway to Norcantharidin-Induced Programmed Cell Death in Human Oral Squamous Cell Carcinoma.
Ahn CH1, Hong KO1, Jin B2, Lee W2, Jung YC3, Lee H4, Shin JA1, Cho SD5, Hong SD6.
2019 Jul 16
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