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).

Caffeic acid modulates histamine-induced reactions. When the concentration of light is increased from 0.1 to 1 mM, the modulatory impact of caffeic acid progressively increases, mimicking a normal dose-modulated response. Capsaicin-induced responses were considerably reduced in HEK293T-TRPV1 cells treated with 1 mM caffeine. Lower doses of caffeic acid inhibit capsaicin-induced reactions. Experiments have shown that caffeic acid can dramatically suppress histamine-sensitive dorsal root ganglion (DRG) neurons. The administration of caffeic acid (1 mM) reduced the percentage of DRG neurons responding to histamine application from 12.5% to 2.1%. The allyl isothiocyanate (AITC)-induced rise in intracellular calcium in TRPA1-expressing cells was thought to be considerably inhibited by 1 mM caffeic acid. Caffeic acid may also inhibit AITC-induced TRPA1 activation [1].

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In HEK293T cells expressing H1R and TRPV1, caffeic acid can significantly block histamine - induced intracellular calcium increase. In primary cultures of mouse dorsal root ganglion (DRG), it also inhibits histamine - induced intracellular calcium increase. In DRG and HEK293T cells expressing MrgprA3 and TrpA1, caffeic acid can inhibit the response induced by chloroquine. Additionally, it can reduce the intracellular calcium changes induced by Sligrl - NH2 in cells via MrgprC11, but it cannot inhibit the response induced by β - alanine via MrgprD.

In the mouse model, histamine-induced scratching (30.50±10.87 times/1 hour, n=6) was seen when caffeic acid (500 mg/kg) was used. Furthermore, although there appeared to be a declining trend (49.40±12.35 times/1 h, n=5), the anti-scratch effect of a lower dose of caffeic acid (100 mg/kg) in histamine-induced scratching was not determined to be significant. Scratching caused by chlorine buffer can be considerably reduced by 500 mg/kg caffeic acid (161.6±31.42 times/1 h, n=5)[1]. In the hippocampal regions, caffeineic acid dramatically decreased 5-LO mRNA (P<0.01). The 5-LO protein expression in the I/R-caffeic acid group was significantly lower (P<0.05 or P<0.01) than in the potential reperfusion (I/R) untreated group. This was particularly true when comparing the I/R-caffeic acid and I/R untreated groups. The latency of finding the platform was significant throughout the process in both the low-dose and high-dose caffeic acid groups, and the entire platform latency was in I/R. Group R-caffeic acid (50 mg/kg). Hippocampal neuron nuclear pyknosis was dramatically reduced in the high-dose caffeic acid group, with a pyknosis rate of (13.3) ±3.0)%, while cell damage was still evident in the low-dose group (63.6±2.8)% [2].

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In a mouse scratching behavior test, caffeic acid has anti - scratching effects against histamine, chloroquine, and Sligrl - NH2 administration. In a rat model of global cerebral ischemia - reperfusion, caffeic acid (10, 30, 50 mg/kg) reduces the escape latency in the Morris water maze, relieves hippocampal neurons injury, and increases neuron count. It also decreases the expression of NF - κBp65 and 5 - LO, reduces malondialdehyde (MDA) content, and increases superoxide dismutase (SOD) activity.

Itch is an unpleasant sensation that evokes a desire to scratch. Although often regarded as a trivial 'alarming' sensation, itch may be debilitating and exhausting, leading to reduction in quality of life. In the current study, the question of whether caffeic acid can be used to alleviate itch sensation induced by various pruritic agents, including histamine, chloroquine, SLIGRL-NH2, and β-alanine was investigated. It turned out that histamine-induced intracellular calcium increase was significantly blocked by caffeic acid in HEK293T cells that express H1R and TRPV1, molecules required for transmission of histamine-induced itch in sensory neurons. In addition, inhibition of histamine-induced intracellular calcium increase by caffeic acid was demonstrated in primary cultures of mouse dorsal root ganglion (DRG). When chloroquine, an anti-malaria agent known to induce histamine-independent itch - was used, it was also found that caffeic acid inhibits the induced response in both DRG and HEK293T cells that express MRGPRA3 and TRPA1, underlying molecular entities responsible for chloroquine-mediated itch. Likewise, intracellular calcium changes by SLIGRL-NH2 - an itch-inducing agent via PAR2 and MRGPRC11 - were decreased by caffeic acid as well. However, it was found that caffeic acid is not capable of inhibiting β-alanine-induced responses via its specific receptor MRGPRD [1].

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For HEK293T cells, they are first transfected to express H1R and TRPV1, then treated with caffeic acid at different concentrations, and finally stimulated with histamine. Intracellular calcium concentration is measured by a calcium - sensitive fluorescent probe. For DRG primary cultures, caffeic acid is added before histamine stimulation, and then the intracellular calcium level is detected in the same way. For cells expressing MrgprA3 and TrpA1 or MrgprC11, the operation is similar, that is, adding caffeic acid first and then stimulating with the corresponding pruritic agents, and finally detecting the change of intracellular calcium.

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

433 to 437 °F (decomposes) (NTP, 1992) ; Decomposes at 223-225 °C (Softens at 194 °C). ; 225 °C

220.0±22.4 °C

0.0±1.0 mmHg at 25°C

1.707

1.42

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

Solubility in Formulation 1: ≥ 2.5 mg/mL (13.88 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (13.88 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 3: ≥ 2.08 mg/mL (11.55 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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 (Please use freshly prepared in vivo formulations for optimal results.)