5-Lipoxygenase (5-LO); TRPV1; Caffeic acid targets histamine receptor H1 (H1R), transient receptor potential vanilloid 1 (TRPV1), Mas - related G - protein coupled receptor A3 (MrgprA3), transient receptor potential ankyrin 1 (TrpA1), Mas - related G - protein coupled receptor C11 (MrgprC11), and 5 - lipoxygenase (5 - LO).

咖啡酸调节组胺诱导的反应。当光浓度从 0.1 mM 增加到 1 mM 时，咖啡酸的调节作用逐渐增强，模拟正常的剂量调节反应。在用 1 mM 咖啡因处理的 HEK293T-TRPV1 细胞中，辣椒素诱导的反应显着降低。较低剂量的咖啡酸可抑制辣椒素引起的反应。实验表明，咖啡酸可以显着抑制组胺敏感的背根神经节（DRG）神经元。施用咖啡酸 (1 mM) 可使对组胺应用做出反应的 DRG 神经元百分比从 12.5% 降低至 2.1%。 1 mM 咖啡酸可显着抑制 TRPA1 表达细胞中异硫氰酸烯丙酯 (AITC) 诱导的细胞内钙升高。咖啡酸还可能抑制 AITC 诱导的 TRPA1 激活 [1]。

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在表达H1R和TRPV1的HEK293T细胞中，咖啡酸可显著阻断组胺诱导的细胞内钙升高。在小鼠背根神经节（DRG）原代培养物中，其也能抑制组胺诱导的细胞内钙升高。在表达MrgprA3和TrpA1的DRG和HEK293T细胞中，咖啡酸可抑制氯喹诱导的反应。此外，它还可降低细胞中由Sligrl - NH2通过MrgprC11诱导的细胞内钙变化，但不能抑制β - 丙氨酸通过MrgprD诱导的反应。

在小鼠模型中，当使用咖啡酸（500 mg/kg）时，观察到组胺诱导的抓挠（30.50±10.87次/1小时，n=6）。此外，虽然似乎有下降趋势（49.40±12.35次/1小时，n=5），但较低剂量咖啡酸（100 mg/kg）在组胺诱导的抓伤中的抗抓伤作用尚未确定具有重要意义。 500 mg/kg 咖啡酸可显着减少氯缓冲液引起的划伤（161.6±31.42 次/1 h，n=5）[1]。在海马区域，咖啡因酸显着降低 5-LO mRNA（P<0.01）。 I/R-咖啡酸组的5-LO蛋白表达显着低于潜在再灌注（I/R）未治疗组（P<0.05或P<0.01）。在比较 I/R-咖啡酸组和 I/R 未治疗组时尤其如此。在低剂量和高剂量咖啡酸组中，整个过程中寻找平台的潜伏期都很显着，并且整个平台潜伏期都在I/R中。 R 组-咖啡酸（50 毫克/千克）。高剂量咖啡酸组海马神经元核固缩明显减少，固缩率为（13.3）±3.0）％，而低剂量组细胞损伤仍然明显（63.6±2.8）％[2] 。

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在小鼠抓挠行为实验中，咖啡酸对组胺、氯喹和Sligrl - NH2诱导的抓挠行为有抑制作用。在大鼠全脑缺血再灌注模型中，咖啡酸（10、30、50 mg/kg）可缩短莫里斯水迷宫中的逃避潜伏期，减轻海马神经元损伤，增加神经元数量。同时降低NF - κBp65和5 - LO的表达，减少丙二醛（MDA）含量，增加超氧化物歧化酶（SOD）活性。

瘙痒是一种令人不快的感觉，会引起抓挠的欲望。尽管瘙痒通常被认为是一种微不足道的“令人担忧”的感觉，但它可能会使人衰弱和疲惫，导致生活质量下降。在目前的研究中，研究了咖啡酸是否可以用于缓解各种瘙痒剂引起的瘙痒感的问题，包括组胺、氯喹、SLIGRL-NH2和β-丙氨酸。事实证明，在表达H1R和TRPV1的HEK293T细胞中，组胺诱导的细胞内钙增加被咖啡酸显著阻断，这些分子是组胺诱导的瘙痒在感觉神经元中传播所需的分子。此外，在小鼠背根神经节（DRG）的原代培养物中，咖啡酸抑制组胺诱导的细胞内钙增加。当使用氯喹（一种已知可诱导组胺非依赖性瘙痒的抗疟疾药物）时，还发现咖啡酸抑制表达MRGPRA3和TRPA1的DRG和HEK293T细胞的诱导反应，这是氯喹介导的瘙痒的潜在分子实体。同样，通过PAR2和MRGPRC11的瘙痒诱导剂SLIGRL-NH2引起的细胞内钙变化也被咖啡酸降低。然而，研究发现，咖啡酸不能通过其特异性受体MRGPRD抑制β-丙氨酸诱导的反应[1]。

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对于HEK293T细胞，先转染使其表达H1R和TRPV1，然后用不同浓度的咖啡酸处理，最后用组胺刺激，通过钙敏感荧光探针检测细胞内钙浓度。对于DRG原代培养物，在组胺刺激前加入咖啡酸，再以同样方式检测细胞内钙水平。对于表达MrgprA3和TrpA1或MrgprC11的细胞，操作类似，即先加入咖啡酸，再用相应的致痒剂刺激，最后检测细胞内钙变化。

Experimental design [2]
Rats were divided into five groups: the sham group (n = 9), I/R non-treated group (n = 9), I/R-caffeic acid group (10 mg · kg−1) (n = 9), I/R-caffeic acid group (30 mg · kg−1) (n = 9) and I/R-caffeic acid group (50 mg · kg−1) (n = 9). In I/R-caffeic acid groups, the rats were administrated caffeic acid at 10, 30, 50 mg · kg−1 (prepared with 0.3% sodium carboxymethyl cellulose) by intraperitoneal injection at 30 min prior to ischemia. The sham group and I/R group were treated with an equal volume of 0.3% sodium carboxymethyl cellulose.

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Induction of global cerebral I/R model[2]
Rats were anesthetized by intraperitoneal injection of chloral hydrate (400 mg/kg), and fixed in a supine position. Global cerebral ischemia was induced as previously described. A midline incision was made in the neck, after that the incision was extended 1 cm to the right. Then both common carotid arteries and the right common jugular vein were exposed carefully by blunt dissection. The distal end of the common jugular vein was ligated following 2 ml heparinized saline (100 mL 0.9% saline containing heparin (250 U)) were perfused. The blood accounting for about 30 percent of the total blood volumes were taken from the right common jugular vein leading to hypotension. Global cerebral ischemia was induced by bilateral clamping of the common carotid arteries combined with hypotension. After ischemia for 20 min, the artery clamps were removed, and the extracted blood was reinfused. Rats in the sham group were subjected to the same operation as above, excepted for the bilateral carotid artery occlusion and hemospasia from the right common jugular vein.

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In the mouse scratching behavior test, caffeic acid is dissolved in an appropriate solvent and administered to mice by gavage. After a certain period, histamine, chloroquine, or Sligrl - NH2 is injected subcutaneously, and the number of scratching times within a specific time is counted. In the rat global cerebral ischemia - reperfusion model, 45 rats are randomly divided into 5 groups: sham group, ischemia - reperfusion non - treated group, and three caffeic acid treatment groups (10, 30, 50 mg/kg). Caffeic acid is dissolved in an appropriate solvent and administered by intraperitoneal injection 30 minutes before bilateral carotid artery occlusion for 20 min, followed by reperfusion. Morris water maze test is carried out after reperfusion, and then hippocampal tissues are collected for HE staining, SOD activity, MDA content detection, and NF - κBp65 expression detection by immunohistochemistry.

Metabolism / Metabolites
The enzymes involved in caffeic acid metabolism have not yet been identified. In the following experiments, caffeic acid (CA), chlorogenic acid (CGA), and dihydrocaffeic acid (DHCA) were incubated with hepatocytes, and the results showed that they can be metabolized by cytochrome P450, catechol-O-methyltransferase (COMT), and β-oxidase. Ferulic acid (FA) or dihydroferulic acid (DHFA), generated by COMT O-methylation of CA or DHCA, can also be O-demethylated by CYP1A1/2, but not by CYP2E1. DHCA or DHFA also undergoes side-chain dehydrogenation reactions to generate CA and FA, respectively, which can be inhibited by thioglycolic acid (an inhibitor of β-oxidase acyl-CoA dehydrogenase). The rate of glutathione conjugate formation catalyzed by NADPH/microsomes (CYP2E1) follows a decreasing order of DHCA > CA > CGA, which is the reverse of the rate of COMT O-methylation. CA and DHCA-o-quinones generated by NADPH/P450 may inhibit COMT, but they can readily form glutathione conjugates. CA, DHCA, and DHFA intermetabolize in isolated rat hepatocytes and can be metabolized to FA, while FA is only metabolized to CA and not to DHCA or DHFA. CA, DHCA, FA, DHFA, and CGA all exhibit dose-dependent hepatotoxicity, with the measured LD50 (2 hours) arranged in decreasing order of toxicity: DHCA > CA > DHFA > CGA > FA. In summary, evidence suggests that O-methylation, GSH conjugation, hydrogenation, and dehydrogenation reactions are all involved in the hepatic metabolism of CA and DHCA. The O-methylation pathway of CA and DHCA is a detoxification pathway, while the P450-catalyzed o-quinone formation pathway is a toxic pathway. In rats, chlorogenic acid is hydrolyzed in the stomach and intestines to caffeic acid and quinic acid. Several metabolites have been identified. Glucuronide of m-coumaric acid and m-hydroxyhippuric acid appears to be the major metabolites in humans. Following oral administration of caffeic acid to human volunteers, O-methylated derivatives (ferulic acid, dihydroferulic acid, and vanillic acid) are rapidly excreted in the urine, while m-hydroxyphenyl derivatives appear later. The dehydroxylation reaction is attributed to the action of intestinal bacteria. Known human metabolites of caffeic acid include (2S,3S,4S,5R)-6-[4-[(E)-2-carboxyvinyl]-2-hydroxyphenoxy]-3,4,5-trihydroxyoxacyclohexane-2-carboxylic acid and (2S,3S,4S,5R)-6-[5-[(E)-2-carboxyvinyl]-2-hydroxyphenoxy]-3,4,5-trihydroxyoxacyclohexane-2-carboxylic acid.

Interactions
Caffeic acid enhanced the uptake of radioglucose by C2C12 cells in a concentration-dependent manner. Phenylephrine had a similar effect on the uptake of radioglucose by C2C12 cells. Prazosin attenuated the effect of caffeic acid, acting in a manner similar to blocking the effect of phenylephrine. Nine-week-old female ICR/Ha mice were fed a diet containing 0.06 mmol/g (10 g/kg diet) of caffeic acid (99% purity). Starting from day 8 of the experiment, mice were administered 1 mg of benzo[a]pyrene twice weekly by gavage for 4 weeks. Three days after the final benzo[a]pyrene treatment, the feeding of caffeic acid-containing diets was discontinued. Mice were sacrificed at 211 days of age. In 17 effective mice, caffeic acid significantly reduced the number of forestomach tumors (≥1 mm) per mouse (histologically undetermined) (p < 0.05) (3.1 tumors per mouse, compared to 5.0 tumors per mouse in 38 mice treated with benzo[a]pyrene alone).

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Antidotes and First Aid Measures
Basic Treatment: Maintain an open airway. Suction if necessary. Observe for signs of respiratory failure and provide assisted ventilation if necessary. Administer oxygen via a non-invasive ventilation mask at a flow rate of 10 to 15 liters per minute. Monitor for pulmonary edema and treat as necessary… Monitor for shock and treat as necessary… If eyes are contaminated, flush with water immediately. During transport, continuously flush each eye with saline… Do not use emetics. If ingested, rinse mouth and dilute with 5 ml/kg to 200 ml of water, provided the patient is able to swallow, has a strong gag reflex, and does not drool. Activated charcoal is ineffective… Do not attempt neutralization, as an exothermic reaction will occur. After decontamination, cover burns with a dry, sterile dressing… /Organic Acids and Related Compounds/ Bronstein, AC, PL Currance; First Aid for Hazardous Substance Exposure. 2nd ed. St. Louis, Missouri. Mosby Lifeline Press. 1994, pp. 152-153.
Advanced Treatment: For patients with altered consciousness, severe pulmonary edema, or respiratory arrest, consider oral or nasal endotracheal intubation to control the airway. Early intubation may be necessary once signs of upper airway obstruction appear. Positive pressure ventilation using a bag-valve-mask may be effective. Monitor heart rhythm and treat arrhythmias if necessary… Establish intravenous access using 5% glucose solution/SRP: “Keep Access Open,” minimum flow rate/. If signs of hypovolemia are present, use lactated Ringer's solution. Be aware of signs of fluid overload. Consider medical treatment for pulmonary edema… For hypotension with signs of hypovolemia, administer fluids with caution. If the patient has normal fluid volume but low blood pressure, consider using vasopressors. Watch for signs of fluid overload… Use promecaine hydrochloride to assist eye irrigation… /Organic Acids and Related Compounds/ Bronstein, AC, PL Currance; Emergency Care for Hazardous Substance Exposure. 2nd ed. St. Louis, Missouri. Mosby Lifeline Press. 1994, p. 100. 153

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Medical Monitoring
Carcinogen Precautions: For those requiring medical monitoring, especially after exposure to carcinogens, provisional decisions should be made regarding potentially useful or mandatory cytogenetic and/or other tests. /Chemical Carcinogens/

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Non-Human Toxicity Excerpt
/Experimental Animals: Subchronic or Chronic Pre-Exposure/ Five six-week-old male Fischer 344 rats were given a basal diet supplemented with 20 g/kg caffeic acid (purity >98%) for four weeks. Epithelial hyperplasia was observed in the forestomach of all treated animals. No hyperplasia was detected in the five untreated control animals. International Agency for Research on Cancer (IARC). Monographs on the Carcinogenic Risk Assessment of Human Chemical Substances. Geneva: World Health Organization, International Agency for Research on Cancer, 1972 to present. (Multi-volume work). Accessible:
/Experimental Animals: Subchronic or Subchronic Exposure/ A group of 15 seven-week-old male Syrian golden hamsters were fed a diet containing 1% (10 g/kg feed) caffeic acid (purity >98%) for 20 weeks. The 1% dose level was chosen as one-quarter of the LD50 for rats. Histopathological and autoradiographic examinations were performed on the stomach and bladder. Mild forestomach hyperplasia was observed in 14 of the 15 treated animals (1 of which was severe), while mild forestomach hyperplasia was observed in 7 of the 15 untreated animals (p < 0.001). Assessment of (3) H-thymidine incorporation showed an increase in the number of labeled cells in the proventriculus, forestomach, and pyloric regions compared with untreated rats, but the difference was not statistically significant. International Agency for Research on Cancer (IARC). Monographs on Risk Assessment of Carcinogenic Chemicals in Humans. Geneva: International Agency for Research on Cancer, World Health Organization, 1972–present. (Multi-volume). Accessible:
/Experimental Animals: Chronic Exposure or Carcinogenicity/ This study investigated the carcinogenic potential of caffeic acid in F344 rats (both male and female) and C57BL/6N x C3H/HeN F1 mice. Thirty animals were fed diets containing 0% and 2.0% caffeic acid, respectively. After 104 weeks of feeding in rats and 96 weeks in mice, detailed histopathological examination revealed a higher incidence of squamous cell papillary carcinoma or cancer in the forestomach of rats (77% in males, 80% in females) and a lower incidence in mice (13% in males, 3% in females). These squamous cell carcinomas were observed to invade the peritoneal cavity in 3 rats and 2 mice. Furthermore, in treated rats, the incidence of renal tubular cell proliferation and adenomas was high (73% and 13% in males, respectively), while it was 20% and 0% in females, respectively, and these lesions were significantly associated with toxic damage. In mice, renal tubular cell proliferation and tumors also appeared in treated female mice (97% and 28%, respectively), while the incidence was lower in male mice (27% and 3%, respectively). No significant nephrotoxic damage was observed in mice. Alveolar type II cell tumors also appeared in treated male mice (27%), which was statistically significant. Therefore, this study demonstrates that caffeic acid has carcinogenic activity against the forestomach squamous cell epithelium of F344 rats and C57BL/6N x C3H/HeN F1 mice (both male and female), renal tubular cells of male rats and female mice, and alveolar type II cells of male mice. PMID:1913684
/Experimental Animals: Chronic Exposure or Carcinogenicity/ Twenty 50-day-old female Sprague-Dawley rats in each group were administered 0.5 ml of 7,12-dimethylbenzo[a]anthracene dissolved in sesame oil at 25 mg/kg body weight via gavage. One week later, the animals were fed a diet containing 0.5% (5 g/kg feed) caffeic acid (purity >99%) for 51 weeks. The mammary glands, ear tubes, stomach, liver, and kidneys were examined. Animals treated with 7,12-dimethylbenzo[a]anthracene alone had a significantly higher incidence of forestomach papillomas (6/19 vs 0/19; p < 0.01). No other significant increases in tumor incidence were observed. International Agency for Research on Cancer (IARC). Monographs on Risk Assessment of Human Carcinogenic Chemicals. Geneva: International Agency for Research on Cancer, World Health Organization, 1972 to present. (Multi-volume). Accessible at: https://monographs.iarc.fr/ENG/Classification/index.php, Volume V56, page 124 (1993).

[1]. Caffeic acid exhibits anti-pruritic effects by inhibition of multiple itch transmission pathways in mice. Eur J Pharmacol. 2015 Sep 5;762:313-21.

[2]. The protective effect of caffeic acid on global cerebral ischemia-reperfusion injury in rats. Behav Brain Funct. 2015 Apr 18;11:18.

According to the International Agency for Research on Cancer (IARC) of the World Health Organization, caffeic acid is potentially carcinogenic. 3,4-Dihydroxycinnamic acid appears as yellow prismatic or flaky forms, or pale yellow granules, in chloroform or petroleum ether solutions. In alkaline solutions, the color changes from yellow to orange. (NTP, 1992) Caffeic acid is a hydroxycinnamic acid formed by replacing the 3 and 4 positions of the benzene ring of cinnamic acid with hydroxyl groups. It exists in both cis and trans forms, with the trans form being more common. Caffeic acid is a plant metabolite and is also an inhibitor of EC 1.13.11.33 (arachidonic acid 15-lipoxygenase), EC 2.5.1.18 (glutathione transferase), EC 1.13.11.34 (arachidonic acid 5-lipoxygenase), an antioxidant, and EC 3.5.1.98 (histone deacetylase). It is a hydroxycinnamic acid belonging to the catechol group of compounds.
It has been reported that caffeic acid is found in Salvia miltiorrhiza, Salvia miltiorrhiza var. albopictus, and other organisms with relevant data.
Caffeic acid is a hydroxycinnamic acid derivative and polyphenol with high oral bioavailability and potential antioxidant, anti-inflammatory, and antitumor activities. After administration, caffeic acid acts as an antioxidant, preventing oxidative stress and thus preventing DNA damage caused by free radicals. Caffeic acid targets and inhibits the histone demethylase (HDM) oncoprotein gene 1 (GASC1; JMJD2C; KDM4C) that amplifies squamous cell carcinoma, thereby inhibiting cancer cell proliferation. GASC1 is a member of the KDM4 subgroup of proteins containing the Jumonji (Jmj) domain. It demethylates lysine 9 and lysine 36 (H3K9 and H3K36) on histone H3 and plays a key role in tumor cell development.
Caffeic acid is a metabolite found or produced in Saccharomyces cerevisiae.
See also: Black cohosh (partial); Lithospermum erythrorhizon root (partial). Burdock root (partial)...View more...

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Mechanism of Action
Caffeic acid phenethyl ester (CAPE) is synthesized from caffeic acid and phenylethanol (ratio 1:5) at room temperature using dicyclohexylcarbodiimide (DCC) as a condensing agent, with a yield of approximately 38%. CAPE inhibits the growth of human leukemia HL-60 cells. It also inhibits the synthesis of DNA, RNA, and proteins in HL-60 cells, with IC50 values of 1.0 M, 5.0 M, and 1.5 M, respectively.
To understand the hypoglycemic effect of caffeic acid, this study used myoblast C2C12 cells to investigate their glucose uptake. Caffeic acid enhanced the uptake of radioactive glucose by C2C12 cells in a concentration-dependent manner. A similar effect of phenylephrine on the uptake of radioactive glucose was also observed in C2C12 cells. Prazosin attenuates the effect of caffeic acid in a similar way to blocking the effect of phenylephrine. The effect of caffeic acid on α1-adrenergic receptors was further confirmed by the binding substitution of [3H]prazosin in C2C12 cells. Furthermore, the glucose uptake-enhancing effect of phenylephrine in C2C12 cells was inhibited by the α1A-adrenergic receptor antagonists tamsulosin and WB 4101, but not by the α1B-adrenergic receptor antagonist chloroethyl clonidine (CEC). Therefore, the presence of α1A-adrenergic receptors in C2C12 cells can be considered. Similar inhibition of caffeic acid effects was also observed in C2C12 cells co-incubated with these antagonists. Activation of α1A-adrenergic receptors appears to be the reason for the action of caffeic acid in C2C12 cells. In the presence of the phospholipase C-specific inhibitor U73312, caffeic acid-stimulated uptake of radioactive glucose into C2C12 cells decreased in a concentration-dependent manner, while U73343 (a negative control of U73312) did not have this effect. Furthermore, chelerythrine and GF 109203X attenuated the effects of caffeic acid at concentrations sufficient to inhibit protein kinase C. Therefore, the data suggest that caffeic acid activation of α1A-adrenergic receptors in C2C12 cells may increase glucose uptake via the phospholipase C-protein kinase C pathway. Studies have shown that 2% dietary caffeic acid (CA, 3,4-dihydroxycinnamic acid) can lead to cancer in the forestomach and kidneys of F344 rats and B6C3F1 mice. Given that caffeic acid is present in coffee and many other foods, and considering the extrapolation of cancer incidence using linear interpolation within a 0% to 2% dose range, the risk of cancer in humans is considerably high. In both target organs, tumor formation precedes proliferation, which may be the primary mechanism of its carcinogenic effect. This study investigated the dose-response relationship of CA (catheterine acid) in male F344 rats after 4 weeks of feeding with different dietary concentrations (0, 0.05%, 0.14%, 0.40%, and 1.64%). Two hours after intraperitoneal injection, immunohistochemical analysis was performed to observe cells in the S phase of DNA replication using incorporated 5-bromo-2'-deoxyuridine (BrdU). In the forestomach, at concentrations of 0.40% and 1.64%, both the total number of epithelial cells per millimeter of slice length and the unit length labeling index (ULLI) of BrdU-positive cells increased by approximately 2.5-fold. No effect was observed at the lowest concentration (0.05%). At a concentration of 0.14%, both indices decreased by approximately one-third. In the kidneys, the labeling index of proximal renal tubular cells also showed a J-shaped (or U-shaped) dose-response, increasing 1.8-fold at 1.64%. No dose-related effects were observed in non-target organs—the proventriculus and liver. Data indicate a strong correlation between cancer-induced organ specificity and cell division stimulation. Linear extrapolation appears inappropriate in terms of dose-response relationships and extrapolating animal tumor data to human cancer risk. Caffeic acid is a phenolic compound widely distributed in medicinal plants. It exerts its antipruritic effect by inhibiting multiple pruritus transmission pathways and has a protective effect against global cerebral ischemia-reperfusion injury in rats, possibly related to inhibition of 5-lipoxygenase (5-LO) and regulation of oxidative stress-related indicators.

C9H8O4

180.1574

180.042

331-39-5

trans-Caffeic acid;501-16-6;Caffeic acid phenethyl ester;104594-70-9;Caffeic acid-13C3;1185245-82-2

689043

Off-white to light yellow solid

1.5±0.1 g/cm3

416.8±35.0 °C at 760 mmHg

211-213 °C (dec.)(lit.)

220.0±22.4 °C

0.0±1.0 mmHg at 25°C

1.707

1.42

77.76

3

4

2

13

212

0

O=C(O)/C=C/C1=CC=C(O)C(O)=C1

QAIPRVGONGVQAS-DUXPYHPUSA-N

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+

(E)-3-(3,4-dihydroxyphenyl)prop-2-enoic acid

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; 2-Propenoic acid, 3-(3,4-dihydroxyphenyl)-;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~555.06 mM)
H2O : < 0.1 mg/mL

配方 1 中的溶解度: ≥ 2.5 mg/mL (13.88 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 25.0 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 2.5 mg/mL (13.88 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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配方 3 中的溶解度: ≥ 2.08 mg/mL (11.55 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 20.8 mg/mL澄清的DMSO储备液加入到400 μL PEG300中，混匀；再向上述溶液中加入50 μL Tween-80，混匀；然后加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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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。