4,4'-Dimethoxychalcone
(Synonyms: 4,4'-甲氧基查耳酮) 目录号 : GC39658
4,4'-Dimethoxychalcone 可从植物当归中分离得到，是一种天然自噬 (autophagy) 诱导剂，具有抗衰老活性。
Cas No.:2373-89-9
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
4,4'-Dimethoxychalcone, isolated from the plant Angelica keiskei koidzumi, acts as a natural autophagy inducer with anti-ageing properties[1].
[1]. Carmona-Gutierrez D, et al. The flavonoid 4,4'-dimethoxychalcone promotes autophagy-dependent longevity across species. Nat Commun. 2019 Feb 19;10(1):651.
| Cas No. | 2373-89-9 | SDF | |
| 别名 | 4,4'-甲氧基查耳酮 | ||
| Canonical SMILES | O=C(C1=CC=C(OC)C=C1)/C=C/C2=CC=C(OC)C=C2 | ||
| 分子式 | C17H16O3 | 分子量 | 268.31 |
| 溶解度 | DMSO: ≥ 250 mg/mL (931.76 mM) | 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 | 3.727 mL | 18.6352 mL | 37.2703 mL |
| 5 mM | 0.7454 mL | 3.727 mL | 7.4541 mL |
| 10 mM | 0.3727 mL | 1.8635 mL | 3.727 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。
Flavonoid 4,4'-Dimethoxychalcone induced ferroptosis in cancer cells by synergistically activating Keap1/Nrf2/HMOX1 pathway and inhibiting FECH
Free Radic Biol Med 2022 Aug 1;188:14-23.PMID:35697292DOI:10.1016/j.freeradbiomed.2022.06.010.
Flavonoids are widely distributed in plants as secondary metabolites and have various biological benefits such as anti-tumor, anti-oxidant, anti-inflammatory and anti-aging. We previously reported that 4,4'-Dimethoxychalcone (DMC) suppressed cancer cell proliferation by aggravating oxidative stress and inducing G2/M cell cycle arrest. In the present study, we explored the underlying mechanisms by which DMC inhibited cancer cell growth. Given that ferrochelatase (FECH) is a potential target of DMC identified by thermal proteome profiling (TPP) method, herein, we confirmed that DMC inhibited the enzymatic activity of FECH. Furthermore, we proved that DMC induced Keap1 degradation via ubiquitin-proteasome system, which led to the nuclear translocation of Nrf2 and upregulated Nrf2 targeted gene HMOX1. FECH inhibition and HMOX1 upregulation resulted in iron overload and triggered ferroptosis in cancer cells. Collectively, we revealed that DMC induced ferroptosis by synergistically activating Keap1/Nrf2/HMOX1 pathway and inhibiting FECH. Our findings indicate that FECH contributes to the non-canonical ferroptosis induction, shed light on the mechanisms of DMC inhibiting cancer cell growth, and set an example for studying biological functions of flavonoids.
4,4'-Dimethoxychalcone increases resistance of mouse oocytes to postovulatory aging in vitro
Reprod Biomed Online 2022 Mar;44(3):411-422.PMID:35153143DOI:10.1016/j.rbmo.2021.12.003.
Research question: Does 4,4'-Dimethoxychalcone (DMC), a natural antioxidant compound, effectively improve the quality of postovulatory ageing (POA) oocytes? Design: Freshly ovulated MII oocytes were cultured in 10-µM DMC for 12 h in vitro. Reactive oxygen species (ROS) production, apoptosis rate, mitochondrial distribution, formation of the actin cap, and fertilization and development potential of POA oocytes, were studied. The change of autophagy level was detected, and the autophagy inhibitor 3-methyladenine (3-MA) was used to establish the relationship between DMC and autophagy. Results: DMC supplementation eliminated the accumulated ROS (P < 0.0001) and ROS dependent 4 hydroxynonenal products (P = 0.0399), and decreased apoptosis (P = 0.0033), reduced abnormal mitochondrion distribution (P = 0.0280), improved mitochondrial membrane potential (P = 0.0135) and restored the formation of the actin cap (P = 0.0487), thus improving fertilization ability (P = 0.0156) and developmental potential (P = 0.0130) in POA oocytes. The role autophagy plays in the effects of DMC supplementation was investigated. The immunofluorescence results showed that POA leads to the accumulation of SQSTM1/p62 (P = 0.0083) but DMC supplementation could eliminate this (P < 0.0001). The western blot result of p62 protein was similar to the immunofluorescence results of the POA group (P = 0.0441) and DMC supplementation group (P = 0.0154). After inhibiting autophagy by 3-MA, the DMC supplementation group could no longer eliminate the accumulation of ROS (P = 0.1704). Conclusions: DMC supplementation activates autophagy to protect oocytes from postovulatory ageing. This approach can feasibly improve the reproductive outcome of ART.
4,4'-Dimethoxychalcone regulates redox homeostasis by targeting riboflavin metabolism in Parkinson's disease therapy
Free Radic Biol Med 2021 Oct;174:40-56.PMID:34332078DOI:10.1016/j.freeradbiomed.2021.07.038.
Oxidative stress damage plays a pivotal role in Parkinson's disease (PD) pathogenesis. Previously, we developed a blood brain barrier-penetrating peptide-based "Trojan Horse" strategy to deliver 4,4'-Dimethoxychalcone (DMC) for PD therapy and revealed neuroprotective properties of DMC in a PD model; however, the underlying mechanisms remained unclear. Here, we report that DMC attenuated motor impairment, degeneration of DA neurons and α-synuclein aggregation in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and exogenous human α-synuclein-induced PD mouse models. Mechanistically, DMC increased the expression of two critical intermediates in riboflavin metabolism: riboflavin kinase (RFK) and its metabolic product, flavin mononucleotide (FMN). We provide the first direct evidence that FMN ameliorated oxidative stress damage and dopaminergic neuron degeneration both in vitro and in vivo and that riboflavin metabolism was required for DMC-mediated neuroprotection. DMC-induced restoration of redox homeostasis was mediated via the activation of protein kinase Cθ (PKCθ) signaling. Together, our findings reveal that DMC may serve as a novel antioxidant in PD intervention and also define a novel mechanism that underlies its therapeutic activity.
Flavonoid 4,4'-Dimethoxychalcone suppresses cell proliferation via dehydrogenase inhibition and oxidative stress aggravation
Free Radic Biol Med 2021 Nov 1;175:206-215.PMID:34506903DOI:10.1016/j.freeradbiomed.2021.09.002.
Flavonoids are natural polyphenolic compounds with a diverse array of biological activities and health-promoting effects. Recent studies have found that 4,4'-Dimethoxychalcone (DMC) promoted longevity via autophagy; however, its targets are currently unknown. Herein, we employed an unbiased thermal proteome profiling (TPP) method and identified multiple targets of DMC, including ALDH1A3, ALDH2, and PTGES2. We further determined the dissociation constant (Kd) of DMC and ALDH1A3 to be 2.8 μM using microscale thermophoresis (MST) analysis, which indicated that DMC inhibited ALDH1A3 activity and aggravated cellular oxidative stress. DMC treatment significantly increased cellular reactive oxygen species (ROS) production and inhibited cancer cell growth. Quantitative proteomic analysis showed that DMC upregulated proteins associated with stress-responses and downregulated proteins associated with cell cycle progression, and this was confirmed using cell cycle analysis. Taken together, we showed that TPP is an effective tool with which to identify flavonoid targets and set a precedent for deciphering flavonoid function in the future. We have demonstrated that DMC inhibited cell proliferation via ROS-induced cell cycle arrest and is an anti-proliferative agent in cancer treatment.