Dibenzoylmethane
(Synonyms: 二苯甲酰甲烷) 目录号 : GC61419
Dibenzoylmethane是甘草中的次要成分，可激活Nrf2并预防各种癌症和氧化损伤。Dibenzoylmethane是姜黄素的类似物，会引起Keap1解离和Nrf2的核易位。
Cas No.:120-46-7
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Dibenzoylmethane, a minor ingredient in licorice, activates Nrf2 and prevents various cancers and oxidative damage. Dibenzoylmethane, an analog of curcumin, results in dissociation from Keap1 and nuclear translocation of Nrf2[1].
Dibenzoylmethane (10, 20, 30, 40, 50 μM; 6 hours) treatment concentration-dependently increases the mRNA level of HO-1 but has no effect on the mRNA level of Nrf2 in HepG2 cells. Dibenzoylmethane induces HO-1 and Nrf2 protein expression, and the induction diminishes after 12 h[1]. Dibenzoylmethane (10, 20, 30, 40, 50 μM; 2 hours) concentration-dependently increases the phosphorylated protein levels of Erk1/2, p38MAPK, JNK, AMPK, and Akt in HepG2 cells.Dibenzoylmethane does not show significant cytotoxicity[1].
Dibenzoylmethane (200, 500 mg/kg/day; ip; for three consecutive days) pretreatment significantly reduces both the area and the severity of necrosis, as well as the leukocyte infiltration, at a dose of 200 mg/kg in wild-type and Nrf2 knockout mice[1]. Dibenzoylmethane protectes against CCl4-induced (1:49,v/v, 10 ml/kg) liver damage in wild-type mice[1].
[1]. Mingnan Cao, et al. Dibenzoylmethane Protects Against CCl4-Induced Acute Liver Injury by Activating Nrf2 via JNK, AMPK, and Calcium Signaling. AAPS J. 2017 Nov;19(6):1703-1714.
| Cas No. | 120-46-7 | SDF | |
| 别名 | 二苯甲酰甲烷 | ||
| Canonical SMILES | O=C(C1=CC=CC=C1)CC(C2=CC=CC=C2)=O | ||
| 分子式 | C15H12O2 | 分子量 | 224.26 |
| 溶解度 | DMSO : 100 mg/mL (445.91 mM; Need ultrasonic) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 4.4591 mL | 22.2955 mL | 44.5911 mL |
| 5 mM | 0.8918 mL | 4.4591 mL | 8.9182 mL |
| 10 mM | 0.4459 mL | 2.2296 mL | 4.4591 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Butyl methoxy Dibenzoylmethane
Profiles Drug Subst Excip Relat Methodol 2013;38:87-111.PMID:23668403DOI:10.1016/B978-0-12-407691-4.00003-4.
A comprehensive profile on Butyl methoxy Dibenzoylmethane, one of the most commonly used ultraviolet (UV) filters in topical sunscreen products, is prepared. This UV filter, often referred to as Avobenzone, has its main absorbance in the UVA I region of the spectrum and is susceptible to photodegradation. The profile contains the following sections: general information, use and mechanism of action, method of preparation, physical characteristics, methods of analysis, stability, and toxicity. The physical characteristics section includes the melting range, differential scanning calorimetry, partition coefficient, ionization constant, solubility, and UV, infrared, nuclear magnetic resonance ((1)H NMR and (13)C NMR) and mass spectrometry and X-ray powder diffractometry. The method of analysis section in addition to compendial identification and purity and assay methods includes thin-layer gas and high-performance liquid chromatography. The photostability and photostabilization of Butyl methoxy Dibenzoylmethane, in addition to its toxicity, are also documented.
Dibenzoylmethane derivative inhibits melanoma cancer in vitro and in vivo through induction of intrinsic and extrinsic apoptotic pathways
Chem Biol Interact 2022 Jan 5;351:109734.PMID:34742685DOI:10.1016/j.cbi.2021.109734.
Malignant melanoma has a low incidence, but is the most lethal type of skin cancer. Studies have shown that dibenzoylmethanes (DBMs) have interesting biological activities, including antineoplastic properties. These findings led us to investigate whether news DBM derivatives exert antitumor effects against skin cancers. In a previous study, we found that 1,3-diphenyl-2-benzyl-1,3-propanedione (DPBP) has high in vitro antineoplastic activity against murine B16F10 melanoma cells, with an IC50 of 6.25 μg/mL. In the current study, we used transdermal and topical formulations of DPBP to evaluate its activity and molecular mechanism of action in a murine model of melanoma. The compound induces tumor cell death with high selectivity (selectivity index of 41.94) by triggering apoptosis through intrinsic and extrinsic pathways. DPBP treatment reduced tumor volume as well as serum VEGF-A and uric acid levels. Hepatomegaly and nephrotoxicity were not observed at the tested doses. Histopathological analysis of sentinel lymph nodes revealed no evidence of metastases. According to the observed data, the DPBP compound was effective for the topical treatment of melanoma cancer, suggesting that it acts as a chemotherapeutic or chemopreventive agent.
Voltammetric and Fluorimetric Studies of Dibenzoylmethane on Glassy Carbon Electrodes and Its Interaction with Tetrakis (3,5-Dicarboxyphenoxy) Cavitand Derivative
Molecules 2022 Dec 26;28(1):185.PMID:36615382DOI:10.3390/molecules28010185.
Due to the medical importance of Dibenzoylmethane, one of the aims of the study was to find an appropriate packing material and a biologically friendly co-solvent to help its introduction into living systems. Accordingly, redox properties of Dibenzoylmethane were investigated on glassy carbon electrodes in acetonitrile and in 1-propanol with cyclic voltammetry, and showed a diffusion-controlled process. In the anodic window, an oxidation peak appeared at around 1.9 V in both solvents. Cycling repeatedly between 0 and 2 V, the reproducibility of this peak was acceptable, but when extending the window to higher potentials, the electrode deactivated, obviously due to electrode material. The addition of the investigated tetrakis(3,5-dicarboxyphenoxy) cavitand did not significantly change the voltammograms. Further electrochemical experiments showed that the coexistence of water in acetonitrile and 1-propanol drastically reduces the solubility of Dibenzoylmethane. Moreover, very rapid electrode deactivation occurred and this fact made the use of electrochemical methods complicated. Considering that both the cavitand and Dibenzoylmethane are soluble in dimethyl sulfoxide, the interaction of these species was investigated and formation of stable complexes was detected. This observation was verified with fluorescence quenching studies. The mixture of water and dimethyl sulphoxide also dramatically improved the solubility of the cavitand-dibenzoylmethane complex at high excess of water. The addition of cavitand improved the solubility of Dibenzoylmethane, a property which supports the application of Dibenzoylmethane in therapy.
Characterization and Systemic Delivery of Dibenzoylmethane via the Intranasal Route
AAPS PharmSciTech 2021 Jan 6;22(1):30.PMID:33404926DOI:10.1208/s12249-020-01904-9.
Intranasal (IN) administration is known to be noninvasive with the potential to carry a drug or vaccine directly to the blood, bypassing first-pass metabolism in the liver and the harsh environment of the gastrointestinal system. Orally administered Dibenzoylmethane (DBM) has been shown experimentally to be neuroprotective in animal models of tauopathy and prion disease and effective in the treatment of certain forms of cancers. The purpose of this study was to prepare, characterize, and test formulations of DBM designed for IN administration. DBM was formulated in brain homogenate (BH) and hypromellose and as nanoparticles (NPs). These formulations were detected using UPLC and characterized in solid and suspension states; NPs were also characterized by in vitro cell culture-based studies. Particle size for DBM NP was 163.8 ± 3.2 nm, and in vitro release studies showed 95.80% of DBM was released from the NPs within 8 days. In vitro cell, culture studies suggested no drug uptake until 6 h. A histological analysis of nasal cavity (NC) sections and blood detection studies were carried out 30 min after inhalation. DBM amounting to 40.77 ± 4.93 and 44.45 ± 5.36 ng/mL was detected in the blood of animals administered DBM in polymeric and NP formulation, respectively. Histological studies on NCs confirmed the presence of BH within lymphatic vessels in the lamina propria of each animal; BH was identified traversing the mucosa in 2 animals. Thus, formulations for DBM administered via IN route were successfully designed and characterized and able to cross the nasal mucosa following inhalation.
Dibenzoylmethane ameliorates lipid-induced inflammation and oxidative injury in diabetic nephropathy
J Endocrinol 2019 Feb 1;240(2):169-179.PMID:30475214DOI:10.1530/JOE-18-0206.
Dibenzoylmethane (DBM) is a beta-diketone analog of curcumin. Numerous studies have shown the beneficial effects of curcumin on diabetes, obesity and diabetic complications including diabetic nephropathy. Recently, we investigated the beneficial metabolic effects of DBM on high-fat diet-induced obesity. However, the effects and mechanisms of action of DBM in the kidney are currently unknown. To investigate the renoprotective effects of DBM in type 2 diabetes, we administered DBM (100 mg/kg) orally for 12 weeks to high-fat diet-induced diabetic model mice. We used mouse renal mesangial (MES13) and macrophage (RAW 264.7) cells to examine the mechanism of action of DBM (20 μM). After DBM treatment, the albumin-to-creatinine ratio was significantly decreased compared to that of the high-fat-diet group. Moreover, damaged renal ultra-structures and functions including increased glomerular volume, glomerular basement membrane thickness and inflammatory signals were ameliorated after DBM treatment. Stimulation of MES13 and RAW264.7 cells by palmitate or high-dose glucose with lipopolysaccharides increased inflammatory signals and macrophage migration. However, these changes were reversed by DBM treatment. In addition, DBM inhibited NADPH oxidase 2 and 4 expression and oxidative DNA damage. Collectively, these data suggested that DBM prevented diabetes-induced renal injury through its anti-inflammatory and antioxidant effects.