trans-Caffeic acid (3,4-dihydroxycinnamic acid (caffeic acid))

别名: Caffeic acid; AI3-63211; caffeic acid; 3,4-Dihydroxycinnamic acid; 331-39-5; 3,4-Dihydroxybenzeneacrylic acid; (E)-3-(3,4-dihydroxyphenyl)prop-2-enoic acid; Cinnamic acid, 3,4-dihydroxy-; 3-(3,4-Dihydroxyphenyl)-2-propenoic acid; ...; 501-16-6; 3,4-二羟基肉桂酸(咖啡酸);Trans-咖啡酸;(2E)-3-(3,4-二羟基苯基)丙烯酸;反式阿魏酸;3,4-二羟基肉桂酸
目录号: V59582 纯度: ≥98%
反式咖啡酸是一种生长刺激剂,可增加生殖组织的伸长生长。
trans-Caffeic acid (3,4-dihydroxycinnamic acid (caffeic acid)) CAS号: 501-16-6
产品类别: Phenols
产品仅用于科学研究,不针对患者销售
规格 价格 库存 数量
100mg
Other Sizes

Other Forms of trans-Caffeic acid (3,4-dihydroxycinnamic acid (caffeic acid)):

  • 咖啡酸
点击了解更多
InvivoChem产品被CNS等顶刊论文引用
产品描述
反式咖啡酸是一种生长刺激剂,可增加生殖组织的伸长生长。
生物活性&实验参考方法
靶点
Microbial Metabolite
体外研究 (In Vitro)
反式咖啡酸对燕麦胚芽鞘 2 毫米切段具有促生长活性。稀溶液的反式咖啡酸可显著促进豌豆上胚轴的直立生长 [1]
药代性质 (ADME/PK)
Metabolism / Metabolites
Enzymes involved in its /caffeic acid/ metabolism have not been identified. In the following, caffeic (CA), chlorogenic (CGA), and dihydrocaffeic (DHCA) acids were incubated with hepatocytes and shown to undergo metabolism by cytochrome P450, catechol-O-methyltransferase (COMT), and beta-oxidation enzymes. Ferulic (FA) or dihydroferulic (DHFA) acids, formed as the result of CA- or DHCA-O-methylation by COMT, were also O-demethylated by CYP1A1/2 but not CYP2E1. DHCA or DHFA also underwent side chain dehydrogenation to form CA and FA, respectively, which was prevented by thioglycolic acid, an inhibitor of the beta-oxidation enzyme acyl CoA dehydrogenase. The rates of glutathione conjugate formation catalyzed by NADPH/microsomes (CYP2E1) in decreasing order DHCA>CA>CGA trend which was in reverse order to the rates of their O-methylation by COMT. The CA- and DHCA-o-quinones formed by NADPH/P450 likely inhibited COMT but can readily form glutathione conjugates. CA, DHCA and DHFA were inter-metabolized to each other and to FA by isolated rat hepatocytes whereas FA was metabolized only to CA but not to DHCA or DHFA. CA, DHCA, FA, DHFA and CGA showed a dose-dependent hepatocyte toxicity and the LD(50) (2 h), determined were in decreasing order of effectiveness DHCA>CA>DHFA>CGA>FA. In summary, evidence has been provided that O-methylation, GSH conjugation, hydrogenation and dehydrogenation are involved in the hepatic metabolism of CA and DHCA. The O-methylation pathway for CA and DHCA is a detoxification route whereas o-quinones formation catalyzed by P450 is the toxification route.
In rats, chlorogenic acid is hydrolysed in the stomach and intestine to caffeic and quinic acids. A number of metabolites have been identified. Glucuronides of meta-coumaric acid and meta-hydroxyhippuric acid appear to be the main metabolites in humans. After oral administration of caffeic acid to human volunteers, O-methylated derivatives (ferulic, dihydroferulic and vanillic acids) were excreted rapidly in the urine, while the meta-hydroxyphenyl derivatives appeared later. The dehydroxylation reactions were ascribed to the action of intestinal bacteria.
Caffeic Acid has known human metabolites that include (2S,3S,4S,5R)-6-[5-[(E)-2-carboxyethenyl]-2-hydroxyphenoxy]-3,4,5-trihydroxyoxane-2-carboxylic acid and (2S,3S,4S,5R)-6-[4-[(E)-2-carboxyethenyl]-2-hydroxyphenoxy]-3,4,5-trihydroxyoxane-2-carboxylic acid.
毒性/毒理 (Toxicokinetics/TK)
Interactions
Caffeic acid enhanced the uptake of radioactive glucose into C2C12 cells in a concentration-dependent manner. Similar effect of phenylephrine on the uptake of radioactive glucose was also observed in C2C12 cells. Prazosin attenuated the action of caffeic acid in a way parallel to the blockade of phenylephrine.
Female ICR/Ha mice, nine weeks of age, were fed a diet containing 0.06 mmol/g (10 g/kg of diet) caffeic acid (purity, 99%). From experimental day 8, the mice were also given 1 mg benzo(a)pyrene by gavage twice a week for four weeks. The diet containing caffeic acid was removed three days after the last benzo(a)pyrene treatment. Mice were killed at 211 days of age. In the 17 effective mice, the number of forestomach tumors (> or = 1 mm)/mouse (histology unspecified) was significantly decreased by caffeic acid (p < 0.05) (3.1 versus 5.0 tumors/mouse among 38 mice treated with benzo(a)pyrene alone).
参考文献

[1]. Vendrig J C, Buffel K. Growth-stimulating activity of trans-caffeic acid isolated from Coleus rhenaltianus. Nature, 1961, 192(4799): 276-277.

其他信息
Caffeic Acid can cause cancer according to The World Health Organization's International Agency for Research on Cancer (IARC).
3,4-dihydroxycinnamic acid appears as yellow prisms or plates (from chloroform or ligroin) or pale yellow granules. Alkaline solutions turn from yellow to orange. (NTP, 1992)
Caffeic acid is a hydroxycinnamic acid that is cinnamic acid in which the phenyl ring is substituted by hydroxy groups at positions 3 and 4. It exists in cis and trans forms; the latter is the more common. It has a role as a plant metabolite, an EC 1.13.11.33 (arachidonate 15-lipoxygenase) inhibitor, an EC 2.5.1.18 (glutathione transferase) inhibitor, an EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor, an antioxidant and an EC 3.5.1.98 (histone deacetylase) inhibitor. It is a hydroxycinnamic acid and a member of catechols.
Caffeic Acid has been reported in Salvia miltiorrhiza, Salvia plebeia, and other organisms with data available.
Caffeic Acid is an orally bioavailable, hydroxycinnamic acid derivative and polyphenol, with potential anti-oxidant, anti-inflammatory, and antineoplastic activities. Upon administration, caffeic acid acts as an antioxidant and prevents oxidative stress, thereby preventing DNA damage induced by free radicals. Caffeic acid targets and inhibits the histone demethylase (HDM) oncoprotein gene amplified in squamous cell carcinoma 1 (GASC1; JMJD2C; KDM4C) and inhibits cancer cell proliferation. GASC1, a member of the KDM4 subgroup of Jumonji (Jmj) domain-containing proteins, demethylates trimethylated lysine 9 and lysine 36 on histone H3 (H3K9 and H3K36), and plays a key role in tumor cell development.
Caffeic acid is a metabolite found in or produced by Saccharomyces cerevisiae.
See also: Black Cohosh (part of); Comfrey Root (part of); Arctium lappa Root (part of) ... View More ...
Mechanism of Action
Caffeic acid phenethyl ester (CAPE) was synthesized from caffeic acid and phenethyl alcohol (ratio 1:5) at room temperature with dicyclohexyl carbodiimide (DCC) as a condensing reagent. The yield was about 38%. CAPE was found to arrest the growth of human leukemia HL-60 cells. It also inhibits DNA, RNA and protein synthesis in HL-60 cells with IC50 of 1.0 M, 5.0 M and 1.5 M, respectively.
In an attempt to understand the antihyperglycemic action of caffeic acid, the myoblast C2C12 cells were employed to investigate the glucose uptake in the present study. Caffeic acid enhanced the uptake of radioactive glucose into C2C12 cells in a concentration-dependent manner. Similar effect of phenylephrine on the uptake of radioactive glucose was also observed in C2C12 cells. Prazosin attenuated the action of caffeic acid in a way parallel to the blockade of phenylephrine. Effect of caffeic acid on alpha1-adrenoceptors was further supported by the displacement of [3H]prazosin binding in C2C12 cells. Moreover, the glucose uptake-increasing action of phenylephrine in C2C12 cells was inhibited by the antagonists of alpha1A-adrenoceptors, both tamsulosin and WB 4101, but not by the antagonist of alpha1B-adrenoceptors, chlorethylclonidine (CEC). The presence of alpha1A-adrenoceptors in C2C12 cells can thus be considered. Similar inhibition of the action of caffeic acid was also obtained in C2C12 cells co-incubating these antagonists. An activation of alpha1A-adrenoceptors seems responsible for the action of caffeic acid in C2C12 cells. In the presence of U73312, the specific inhibitor of phospholipase C, caffeic acid-stimulated uptake of radioactive glucose into C2C12 cells was reduced in a concentration-dependent manner and it was not affected by U73343, the negative control of U73312. Moreover, chelerythrine and GF 109203X diminished the action of caffeic acid at concentrations sufficient to inhibit protein kinase C. Therefore, the obtained data suggest that an activation of alpha1A-adrenoceptors in C2C12 cells by caffeic acid may increase the glucose uptake via phospholipase C-protein kinase C pathway.
Caffeic acid (CA, 3,4-dihydroxycinnamic acid), at 2% in the diet, had been shown to be carcinogenic in forestomach and kidney of F344 rats and B6C3F1 mice. Based on its occurrence in coffee and numerous foods and using a linear interpolation for cancer incidence between dose 0 and 2%, the cancer risk in humans would be considerable. In both target organs, tumor formation was preceded by hyperplasia, which could represent the main mechanism of carcinogenic action. The dose-response relationship for this effect was investigated in male F344 rats after 4-week feeding with CA at different dietary concentrations (0, 0.05, 0.14, 0.40, and 1.64%). Cells in S-phase of DNA replication were visualized by immunohistochemical analysis of incorporated 5-bromo-2'-deoxyuridine (BrdU), 2 hr after intraperitoneal injection. In the forestomach, both the total number of epithelial cells per millimeter section length and the unit length labeling index of BrdU-positive cells (ULLI) were increased, about 2.5-fold, at 0.40 and 1.64%. The lowest concentration (0.05%) had no effect. At 0.14%, both variables were decreased by about one-third. In the kidney, the labeling index in proximal tubular cells also indicated a J-shaped (or U-shaped) dose response with a 1.8-fold increase at 1.64%. In the glandular stomach and in the liver, which are not target organs, no dose-related effect was seen. The data show a good correlation between the organ specificity for cancer induction and stimulation of cell division. With respect to the dose-response relationship and the corresponding extrapolation of the animal tumor data to a human cancer risk, a linear extrapolation appears not to be appropriate.
Trans - Caffeic acid may be a very important natural growth regulator, which has a growth - promoting effect similar to indole - 3 - acetic acid. It is one of the active growth substances in the ether extract of Coleus rhenaltianus leaves [1]
*注: 文献方法仅供参考, InvivoChem并未独立验证这些方法的准确性
化学信息 & 存储运输条件
分子式
C9H8O4
分子量
180.16
精确质量
180.042
元素分析
C, 60.00; H, 4.48; O, 35.52
CAS号
501-16-6
相关CAS号
Caffeic acid; 331-39-5
PubChem CID
689043
外观&性状
White to off-white solid powder
密度
1.5±0.1 g/cm3
沸点
416.8±35.0 °C at 760 mmHg
熔点
211-213ºC (dec.)(lit.)
闪点
220.0±22.4 °C
蒸汽压
0.0±1.0 mmHg at 25°C
折射率
1.707
LogP
1.42
tPSA
77.76
氢键供体(HBD)数目
3
氢键受体(HBA)数目
4
可旋转键数目(RBC)
2
重原子数目
13
分子复杂度/Complexity
212
定义原子立体中心数目
0
SMILES
C1=CC(=C(C=C1/C=C/C(=O)O)O)O
InChi Key
QAIPRVGONGVQAS-DUXPYHPUSA-N
InChi Code
InChI=1S/C9H8O4/c10-7-3-1-6(5-8(7)11)2-4-9(12)13/h1-5,10-11H,(H,12,13)/b4-2+
化学名
(E)-3-(3,4-dihydroxyphenyl)prop-2-enoic acid
别名
Caffeic acid; AI3-63211; caffeic acid; 3,4-Dihydroxycinnamic acid; 331-39-5; 3,4-Dihydroxybenzeneacrylic acid; (E)-3-(3,4-dihydroxyphenyl)prop-2-enoic acid; Cinnamic acid, 3,4-dihydroxy-; 3-(3,4-Dihydroxyphenyl)-2-propenoic acid; ...; 501-16-6;
HS Tariff Code
2934.99.9001
存储方式

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

运输条件
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
溶解度数据
溶解度 (体外实验)
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
溶解度 (体内实验)
注意: 如下所列的是一些常用的体内动物实验溶解配方,主要用于溶解难溶或不溶于水的产品(水溶度<1 mg/mL)。 建议您先取少量样品进行尝试,如该配方可行,再根据实验需求增加样品量。

注射用配方
(IP/IV/IM/SC等)
注射用配方1: DMSO : Tween 80: Saline = 10 : 5 : 85 (如: 100 μL DMSO 50 μL Tween 80 850 μL Saline)
*生理盐水/Saline的制备:将0.9g氯化钠/NaCl溶解在100 mL ddH ₂ O中,得到澄清溶液。
注射用配方 2: DMSO : PEG300Tween 80 : Saline = 10 : 40 : 5 : 45 (如: 100 μL DMSO 400 μL PEG300 50 μL Tween 80 450 μL Saline)
注射用配方 3: DMSO : Corn oil = 10 : 90 (如: 100 μL DMSO 900 μL Corn oil)
示例: 注射用配方 3 (DMSO : Corn oil = 10 : 90) 为例说明, 如果要配制 1 mL 2.5 mg/mL的工作液, 您可以取 100 μL 25 mg/mL 澄清的 DMSO 储备液,加到 900 μL Corn oil/玉米油中, 混合均匀。
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注射用配方 4: DMSO : 20% SBE-β-CD in Saline = 10 : 90 [如:100 μL DMSO 900 μL (20% SBE-β-CD in Saline)]
*20% SBE-β-CD in Saline的制备(4°C,储存1周):将2g SBE-β-CD (磺丁基-β-环糊精) 溶解于10mL生理盐水中,得到澄清溶液。
注射用配方 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (如: 500 μL 2-Hydroxypropyl-β-cyclodextrin (羟丙基环胡精) 500 μL Saline)
注射用配方 6: DMSO : PEG300 : Castor oil : Saline = 5 : 10 : 20 : 65 (如: 50 μL DMSO 100 μL PEG300 200 μL Castor oil 650 μL Saline)
注射用配方 7: Ethanol : Cremophor : Saline = 10: 10 : 80 (如: 100 μL Ethanol 100 μL Cremophor 800 μL Saline)
注射用配方 8: 溶解于Cremophor/Ethanol (50 : 50), 然后用生理盐水稀释。
注射用配方 9: EtOH : Corn oil = 10 : 90 (如: 100 μL EtOH 900 μL Corn oil)
注射用配方 10: EtOH : PEG300Tween 80 : Saline = 10 : 40 : 5 : 45 (如: 100 μL EtOH 400 μL PEG300 50 μL Tween 80 450 μL Saline)


口服配方
口服配方 1: 悬浮于0.5% CMC Na (羧甲基纤维素钠)
口服配方 2: 悬浮于0.5% Carboxymethyl cellulose (羧甲基纤维素)
示例: 口服配方 1 (悬浮于 0.5% CMC Na)为例说明, 如果要配制 100 mL 2.5 mg/mL 的工作液, 您可以先取0.5g CMC Na并将其溶解于100mL ddH2O中,得到0.5%CMC-Na澄清溶液;然后将250 mg待测化合物加到100 mL前述 0.5%CMC Na溶液中,得到悬浮液。
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口服配方 3: 溶解于 PEG400 (聚乙二醇400)
口服配方 4: 悬浮于0.2% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 5: 溶解于0.25% Tween 80 and 0.5% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 6: 做成粉末与食物混合


注意: 以上为较为常见方法,仅供参考, InvivoChem并未独立验证这些配方的准确性。具体溶剂的选择首先应参照文献已报道溶解方法、配方或剂型,对于某些尚未有文献报道溶解方法的化合物,需通过前期实验来确定(建议先取少量样品进行尝试),包括产品的溶解情况、梯度设置、动物的耐受性等。

请根据您的实验动物和给药方式选择适当的溶解配方/方案:
1、请先配制澄清的储备液(如:用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液,按从左到右的顺序依次添加助溶剂,澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明,并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中,混合均匀/澄清;向上述体系中加入50 μL Tween-80,混合均匀/澄清;然后继续加入450 μL ddH2O (或 saline)定容至 1 mL;

3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出,可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果,工作液请现配现用!
6、如不确定怎么将母液配置成体内动物实验的工作液,请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。
制备储备液 1 mg 5 mg 10 mg
1 mM 5.5506 mL 27.7531 mL 55.5062 mL
5 mM 1.1101 mL 5.5506 mL 11.1012 mL
10 mM 0.5551 mL 2.7753 mL 5.5506 mL

1、根据实验需要选择合适的溶剂配制储备液 (母液):对于大多数产品,InvivoChem推荐用DMSO配置母液 (比如:5、10、20mM或者10、20、50 mg/mL浓度),个别水溶性高的产品可直接溶于水。产品在DMSO 、水或其他溶剂中的具体溶解度详见上”溶解度 (体外)”部分;

2、如果您找不到您想要的溶解度信息,或者很难将产品溶解在溶液中,请联系我们;

3、建议使用下列计算器进行相关计算(摩尔浓度计算器、稀释计算器、分子量计算器、重组计算器等);

4、母液配好之后,将其分装到常规用量,并储存在-20°C或-80°C,尽量减少反复冻融循环。

计算器

摩尔浓度计算器可计算特定溶液所需的质量、体积/浓度,具体如下:

  • 计算制备已知体积和浓度的溶液所需的化合物的质量
  • 计算将已知质量的化合物溶解到所需浓度所需的溶液体积
  • 计算特定体积中已知质量的化合物产生的溶液的浓度
使用摩尔浓度计算器计算摩尔浓度的示例如下所示:
假如化合物的分子量为350.26 g/mol,在5mL DMSO中制备10mM储备液所需的化合物的质量是多少?
  • 在分子量(MW)框中输入350.26
  • 在“浓度”框中输入10,然后选择正确的单位(mM)
  • 在“体积”框中输入5,然后选择正确的单位(mL)
  • 单击“计算”按钮
  • 答案17.513 mg出现在“质量”框中。以类似的方式,您可以计算体积和浓度。

稀释计算器可计算如何稀释已知浓度的储备液。例如,可以输入C1、C2和V2来计算V1,具体如下:

制备25毫升25μM溶液需要多少体积的10 mM储备溶液?
使用方程式C1V1=C2V2,其中C1=10mM,C2=25μM,V2=25 ml,V1未知:
  • 在C1框中输入10,然后选择正确的单位(mM)
  • 在C2框中输入25,然后选择正确的单位(μM)
  • 在V2框中输入25,然后选择正确的单位(mL)
  • 单击“计算”按钮
  • 答案62.5μL(0.1 ml)出现在V1框中
g/mol

分子量计算器可计算化合物的分子量 (摩尔质量)和元素组成,具体如下:

注:化学分子式大小写敏感:C12H18N3O4  c12h18n3o4
计算化合物摩尔质量(分子量)的说明:
  • 要计算化合物的分子量 (摩尔质量),请输入化学/分子式,然后单击“计算”按钮。
分子质量、分子量、摩尔质量和摩尔量的定义:
  • 分子质量(或分子量)是一种物质的一个分子的质量,用统一的原子质量单位(u)表示。(1u等于碳-12中一个原子质量的1/12)
  • 摩尔质量(摩尔重量)是一摩尔物质的质量,以g/mol表示。
/

配液计算器可计算将特定质量的产品配成特定浓度所需的溶剂体积 (配液体积)

  • 输入试剂的质量、所需的配液浓度以及正确的单位
  • 单击“计算”按钮
  • 答案显示在体积框中
动物体内实验配方计算器(澄清溶液)
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)
第二步:请输入动物体内配方组成(配方适用于不溶/难溶于水的化合物),不同的产品和批次配方组成不同,如对配方有疑问,可先联系我们提供正确的体内实验配方。此外,请注意这只是一个配方计算器,而不是特定产品的确切配方。
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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)。如该浓度超过该批次药物DMSO溶解度,请首先与我们联系。

体内配方配制方法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 ddH2O,混匀澄清。

(1) 请确保溶液澄清之后,再加入下一种溶剂 (助溶剂) 。可利用涡旋、超声或水浴加热等方法助溶;
            (2) 一定要按顺序加入溶剂 (助溶剂) 。

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