4-Hydroxychalcone
(Synonyms: 2-羟基查耳酮) 目录号 : GC38663
A chalcone metabolite with diverse biological activities
Cas No.:20426-12-4
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
4'-hydroxy Chalcone is a chalcone metabolite with diverse biological activities. It is formed when chalcone is metabolized by the cytochrome (CYP) P450 isoform CYP1A1 or CYP2C6.1 4'-hydroxy Chalcone is estrogenic in MCF-7 cells and is cytotoxic at concentrations higher than 100 nM. It inhibits TNF-α-induced NF-κB signaling and the trypsin-, chymotrypsin-, and caspase-like proteolytic activities of the 26S proteasome in K562 cells in a dose-dependent manner.2 4'-hydroxy Chalcone reduces growth of K562, U937, and Jurkat cancer cell lines in a dose-dependent manner without effecting viability of peripheral blood mononuclear cells (PBMCs). It also inhibits glutathione reductase (GSH-RD; IC50 = 47.3 μM) in vitro in a reversible and non-competitive manner.3
1.Kohno, Y., Kitamura, S., Sanoh, S., et al.Metabolism of the α,β-unsaturated ketones, chalcone and trans-4-phenyl-3-buten-2-one, by rat liver microsomes and estrogenic activity of the metabolitesDrug Metab. Dispos.33(8)1115-1123(2005) 2.Orlikova, B., Tasdemir, D., Golais, F., et al.The aromatic ketone 4'-hydroxychalcone inhibits TNFα-induced NF-κB activation via proteasome inhibitionBiochem. Pharmacol.82(6)620-631(2011) 3.Zhang, K., Yang, E.-B., Tang, W.-Y., et al.Inhibition of glutathione reductase by plant polyphenols.Biochem. Pharmacol.54(9)1047-1053(1997)
| Cas No. | 20426-12-4 | SDF | |
| 别名 | 2-羟基查耳酮 | ||
| Canonical SMILES | O=C(C1=CC=CC=C1)/C=C/C2=CC=C(O)C=C2 | ||
| 分子式 | C15H12O2 | 分子量 | 224.25 |
| 溶解度 | DMSO: ≥ 250 mg/mL (1114.83 mM) | 储存条件 | 4°C, protect from light |
| 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 | 4.4593 mL | 22.2965 mL | 44.5931 mL |
| 5 mM | 0.8919 mL | 4.4593 mL | 8.9186 mL |
| 10 mM | 0.4459 mL | 2.2297 mL | 4.4593 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。
Effect of 4-Hydroxychalcone as preventive and curative treatment in Wistar rats with liver injury
Can J Physiol Pharmacol 2022 Oct 1;100(10):1005-1017.PMID:35985049DOI:10.1139/cjpp-2021-0628.
The increasing prevalence and complications related to liver diseases (caused by infection, toxic agents, or metabolic syndrome), together with insufficient existence of treatments, make evident the need for better therapeutic alternatives. Therefore, the aim of this study was to determine the effect of 4-Hydroxychalcone (4-HC) as preventive and curative treatment in acute and chronic liver injury, respectively. Liver damage was induced with carbon tetrachloride (CCl4) in Wistar rats. Rats were divided into two groups: (1) acute liver injury and (2) chronic liver injury. In turn, each group was divided into four subgroups: (i) control (water); (ii) dimethyl sulfoxide 10%; (iii) CCl4; and (iv) 4-HC. The pre-treatment with 4-HC decreased transaminases, IL-6 serum levels, and hepatic malondialdehyde, increased IL-10 serum levels and hepatic glutathione, and decreased liver damage (necrosis, steatosis, and inflammatory infiltrate). In contrast, treatment with 4-HC after the induction of chronic liver injury decreased IL-6 serum levels and liver damage (steatosis, inflammatory infiltrate, ballooning cells, steatofibrosis, and fibrosis degree). Thus, the 4-HC treatment is proposed as a preventive treatment against acute liver injury; moreover, these results suggested the potential of 4-HC as a curative treatment against chronic liver injury, but other scheme treatments must be evaluated in future.
4-Hydroxychalcone Induces Cell Death via Oxidative Stress in MYCN-Amplified Human Neuroblastoma Cells
Oxid Med Cell Longev 2019 Dec 5;2019:1670759.PMID:31885773DOI:10.1155/2019/1670759.
Neuroblastoma is an embryonal malignancy that arises from cells of sympathoadrenal lineage during the development of the nervous system. It is the most common pediatric extracranial solid tumor and is responsible for 15% of childhood deaths from cancer. Fifty percent of cases are diagnosed as high-risk metastatic disease with a low overall 5-year survival rate. More than half of patients experience disease recurrence that can be refractory to treatment. Amplification of the MYCN gene is an important prognostic indicator that is associated with rapid disease progression and a poor prognosis, highlighting the need for new therapeutic approaches. In recent years, there has been an increasing focus on identifying anticancer properties of naturally occurring chalcones, which are secondary metabolites with variable phenolic structures. Here, we report that 4-Hydroxychalcone is a potent cytotoxin for MYCN-amplified IMR-32 and SK-N-BE (2) neuroblastoma cells, when compared to non-MYCN-amplified SH-SY5Y neuroblastoma cells and to the non-neuroblastoma human embryonic kidney cell line, HEK293t. Moreover, 4-Hydroxychalcone treatment significantly decreased cellular levels of the antioxidant glutathione and increased cellular reactive oxygen species. In addition, 4-Hydroxychalcone treatment led to impairments in mitochondrial respiratory function, compared to controls. In support of this, the cytotoxic effect of 4-Hydroxychalcone was prevented by co-treatment with either the antioxidant N-acetyl-L-cysteine, a pharmacological inhibitor of oxidative stress-induced cell death (IM-54) or the mitochondrial reactive oxygen species scavenger, Mito-TEMPO. When combined with the anticancer drugs cisplatin or doxorubicin, 4-Hydroxychalcone led to greater reductions in cell viability than was induced by either anti-cancer agent alone. In summary, this study identifies a cytotoxic effect of 4-Hydroxychalcone in MYCN-amplified human neuroblastoma cells, which rationalizes its further study in the development of new therapies for pediatric neuroblastoma.
4-Hydroxychalcone attenuates hyperaldosteronism, inflammation, and renal injury in cryptochrome-null mice
Biomed Res Int 2014;2014:603415.PMID:25003119DOI:10.1155/2014/603415.
In the present study, we aimed to investigate the preventive effects of 4-Hydroxychalcone (4HCH) on resistant hypertension. We used cryptochrome-null mice, which characteristically show high plasma aldosterone levels, inflammation, and renal injury. The cryptochrome-null mice received high-salt treatment and were treated orally with 4HCH 10 mg/kg, 4HCH 20 mg/kg, and 4HCH 40 mg/kg, respectively. The salt administration in cryptochrome-null mice is able to induce an increase in systolic pressure which is associated with hyperaldosteronism, inflammation, and kidney injury. Treatment with 40 mg/kg 4HCH reduced systolic hypertension, serum IL-1β, and TNF-α levels and suppressed the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and renal injury. The impact of 4HCH on the hyperaldosteronism, inflammation, and kidney injury provides new insights for future development of therapeutic strategies in resistant hypertension.
Therapeutic effect of treatment with metformin and/or 4-Hydroxychalcone in male Wistar rats with nonalcoholic fatty liver disease
Eur J Pharmacol 2019 Nov 15;863:172699.PMID:31563650DOI:10.1016/j.ejphar.2019.172699.
Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease in the world. Despite the impact of this pathology in the population, nowadays there is no specific treatment for this disease, focusing its treatment on risks factors. However, it is imperative the existence of a specific treatment, due to this, the aim of this study was to determine the therapeutic effect of treatment with metformin, 4-Hydroxychalcone or co-treatment on male Wistar rats with NAFLD. Wistar rats were divided into two groups with free access to either tap water or 50% sucrose (NAFLD) during 25 weeks. After 20 weeks of induction each were divided into four groups that received daily p.o. administration of: i) saline solution (1 ml); ii) metformin (200 mg/kg/day); iii) 4-Hydroxychalcone (80 mg/kg/day) and i.v.) co-treatment (metformin plus 4-Hydroxychalcone at the doses mentioned above), for 5 weeks. In healthy rats: metformin and co-treatment modified food and total caloric intake and induced diarrhea; but none of the treatments changed the other parameters evaluated. Meanwhile in rats with NAFLD: i) metformin inhibited hepatic total cholesterol and TGF-β, increased diarrhea frequency, and slightly decreased liver steatosis, and fibrosis; ii) 4-Hydroxychalcone decreased IL-6, TNF-α and TGF-β, increased IL-10, and markedly decreased liver steatosis and fibrosis; and iii) co-treatment markedly decreased food intake, total caloric intake, and body weight, increased diarrhea; increased IL-10, showing and intermediate effect on decrease TNF-α, TGF-β, liver steatosis and fibrosis. Our results showed that 4-Hydroxychalcone treatment was the most effective among the treatments tested against NAFLD.
4-Hydroxyhalcone effects on cisplatin-induced genotoxicity model
Toxicol Res (Camb) 2021 Jan 5;10(1):11-17.PMID:33613968DOI:10.1093/toxres/tfaa091.
Background: The genotoxicity of cisplatin (CP) as a platinum-based antineoplastic agent due to its oxidative stress induction was well known. In this research, we examined 4-Hydroxychalcone (4-HCH) as a natural food that presents flavonoid effects on reactive oxygen species (ROS) production and CP-induced in vivo genotoxicity. Method and materials: Cytotoxicity of CP and 4-HCH was measured on human embryonic kidney 293 cells with MTT assay. Then, intracellular ROS content at IC50 concentration of CP was measured with 2',7'-dichlorofluorescein diacetate (DCFDA) dye. Finally, 4-HCH was administered intraperitoneally at 10 and 40 mg/kg/BW doses as a pre and post-treatment schedule in a mice model of CP genotoxicity (7 mg/kg). Acridine-orange-stained bone marrow cells were quantified for micronucleus presence examination. Results: The calculated IC50 of CP and 4-HCH were reported around 19.4 and 133.6 μM, respectively, on HEK293 cells. Also, it was observed that 4-HCH at 0.2, 2 and 10 μM concentrations did not show obvious cytotoxicity. The fluorimetry confirmed that pre-treatment with 10 μM and co-treatment with 2 μM of 4-HCH could attenuate the CP-induced ROS production (P < 0.05 and P < 0.01, respectively). Also, the lowest micronucleated cells were seen in 10 mg/kg 4-HCH-treated group after CP exposure (39 ± 7.9, P < 0.0001). Discussion: Our results demonstrated the antigenotoxic action of 4-HCH in CP-treated mice bone marrow cells for the first time in both concentrations of 10 and 40 mg/kg especially in the form of co-treatment. Further studies required clinical application of this compound in a combination of CP to attenuate the normal cells' genotoxicity side effects.