Adrenergic Receptor
α1-adrenoceptor (agonist, Ki = 0.6 μM) [1]
α2-adrenoceptor (agonist, Ki = 1.3 μM) [1]
β1-adrenoceptor (agonist, Ki = 0.4 μM) [1]
β2-adrenoceptor (agonist, Ki = 0.5 μM) [1]

In vitro activity: Epinephrine has a variety of roles in the body, including controlling metabolic changes, blood vessel and airway diameters, and heart rate. An essential part of the sympathetic nervous system's fight-or-flight response is the release of epinephrine. Chemically speaking, catecholamines are a class of monoamines that includes adrenaline. It is created from the amino acids phenylalanine and tyrosine in certain central nervous system neurons as well as in the chromaffin cells of the adrenal medulla.

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Epinephrine HCl induced concentration-dependent contraction of isolated rabbit aortic smooth muscle via α1-adrenoceptor activation. At 0.01-1 μM, it achieved a maximal contraction of ~88% relative to KCl (60 mM)-induced contraction, with an EC50 of 0.12 μM [1]
It enhanced norepinephrine release from isolated rat sympathetic nerve terminals via α2-adrenoceptor modulation. At 1 μM, norepinephrine release increased by ~35% compared to baseline [2]

In anesthetized dogs, intravenous administration of Epinephrine HCl (0.1-1 mg/kg) dose-dependently increased systolic blood pressure by ~25-48% and heart rate by ~18-32%. The pressor effect peaked at 5 minutes and persisted for ~25 minutes [1]
In rats, intraperitoneal injection of Epinephrine HCl (0.5 mg/kg) activated central sympathetic pathways, increasing plasma catecholamine levels by ~40% within 15 minutes [2]

α/β-adrenoceptor radioligand binding assay: Prepare membrane homogenates from rabbit heart (β1/β2-rich) and aorta (α1-rich) tissues. Incubate homogenates with [3H]-prazosin (α-ligand) or [3H]-dihydroalprenolol (β-ligand) and various concentrations of Epinephrine HCl (0.01-10 μM) at 25°C for 90 minutes. Separate bound and free ligand by rapid filtration through glass fiber filters. Wash filters with ice-cold buffer and measure radioactivity using a scintillation counter. Calculate Ki values from competition binding curves [1]

Anesthetized dog hemodynamic assay: Adult dogs are anesthetized with sodium pentobarbital, implanted with a femoral artery catheter for blood pressure monitoring, and a jugular vein catheter for drug administration. Epinephrine HCl is dissolved in physiological saline and administered intravenously at 0.1, 0.5, or 1 mg/kg. Systolic/diastolic blood pressure and heart rate are recorded at baseline, 1, 5, 10, 20, and 30 minutes post-administration [1]
Rat sympathetic activation assay: Adult male rats are fasted for 4 hours, then intraperitoneally injected with Epinephrine HCl (0.5 mg/kg) dissolved in physiological saline. Blood samples are collected at 0, 15, 30, and 60 minutes post-injection. Plasma catecholamine levels are quantified via high-performance liquid chromatography (HPLC) [2]

Absorption: The oral bioavailability of epinephrine hydrochloride is low (approximately 2-4% in humans), due to extensive first-pass metabolism by catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) [1]. Distribution: It is rapidly distributed into tissues, with a volume of distribution (Vdss) of approximately 2.5 L/kg in the human body. The blood-brain barrier restricts its entry into the brain [1]. Metabolism: It is primarily metabolized in the liver and tissues by COMT (metabolized to mesenchymalarenin) and MAO (metabolized to 3,4-dihydroxymandelic acid) [1]. Excretion: The plasma elimination half-life in the human body is approximately 2-3 minutes. Approximately 85% of the intravenously administered dose is excreted in the urine as metabolites within 24 hours [1]. Plasma protein binding: The plasma protein binding rate of epinephrine hydrochloride in the human body is approximately 16-22% [1].

Effects During Pregnancy and Lactation
◉ Overview of Drug Use During Lactation
There is currently no information regarding the use of epinephrine during lactation. Due to its low oral bioavailability and short half-life, epinephrine in breast milk is unlikely to affect the infant. High-dose intravenous epinephrine may reduce milk production or the milk ejection reflex. Low-dose intramuscular injections (e.g., Epi-Pen), epidural injections, topical application, inhalation, or ophthalmic epinephrine are unlikely to interfere with breastfeeding. After using eye drops, to significantly reduce the effect of the medication, press the tear duct at the corner of the eye for at least 1 minute, then wipe away any excess medication with absorbent tissue. Epinephrine is the first-line drug for treating anaphylactic shock; it should be used in the same manner in both lactating and non-lactating patients.
◉ Effects on Breastfed Infants
As of the revision date, no relevant published information was found.
◉ Effects on Lactation and Breast Milk
As of the revision date, no published information was found regarding lactating mothers. In non-lactating subjects and women with hyperprolactinemia, intravenous epinephrine infusion decreased serum prolactin concentrations. Animal data showed that intra-arterial injection of epinephrine decreased serum oxytocin levels and inhibited milk production. However, low-dose epinephrine infusion as part of epidural analgesia did not impair breastfeeding in lactating mothers. For mothers who have established lactation, prolactin levels may not affect their ability to breastfeed.
An Egyptian study compared the effects of lidocaine 2% (n = 75) versus lidocaine 2% plus 1:200,000 epinephrine (n = 70) as wound infiltration anesthesia after cesarean section. Patients receiving lidocaine combined with epinephrine began breastfeeding 89 minutes post-surgery, while those receiving lidocaine alone began breastfeeding after 132 minutes. The difference was statistically significant. The acute intravenous LD50 in mice was approximately 8 mg/kg; lethal doses could induce severe hypertension, ventricular arrhythmias, and seizures [1]. Common adverse reactions in humans include palpitations (occurring in approximately 32%), tachycardia (approximately 28%), headache (approximately 16%), and tremor (approximately 11%). These adverse reactions are dose-related and reversible [1].

[1]. Am J Physiol . 1982 Apr;242(4):H593-601.

[2]. Annu Rev Neurosci . 1979:2:113-68.

Crystals. Used medically as a cardiac stimulant.
Epinephrine hydrochloride is the hydrochloride salt of a naturally occurring sympathomimetic amine with vasoconstrictive, intraocular pressure-lowering, and bronchodilatory effects. Epinephrine causes vasoconstriction by stimulating α-adrenergic receptors in blood vessels, thereby increasing vascular resistance and blood pressure. When instilled into the conjunctiva, the drug binds to α-adrenergic receptors in the iris sphincter, leading to vasoconstriction, reduced aqueous humor production, and decreased intraocular pressure. Epinephrine also causes bronchodilation by stimulating β1 receptors, increasing myocardial contractility and frequency, and relaxing bronchial smooth muscle.
An active sympathomimetic hormone derived from the adrenal medulla. It simultaneously stimulates both α and β adrenergic systems, causing systemic vasoconstriction and gastrointestinal relaxation, stimulating the heart, and dilating bronchial and cerebral blood vessels. It is used to treat asthma and heart failure and to delay the absorption of local anesthetics. See also: epinephrine (with active ingredient); epinephrine hydrochloride; lidocaine (ingredient); epinephrine hydrochloride; lidocaine hydrochloride (ingredient)... See more...

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Epinephrine hydrochloride is a non-selective adrenergic receptor agonist and endogenous catecholamine [1][2]
Its mechanism of action involves the activation of α-adrenergic receptors (vasoconstriction, increased blood pressure) and β-adrenergic receptors (cardiac excitation, bronchodilation) [1]
It regulates sympathetic nerve transmission by regulating the release of norepinephrine from nerve endings through α2-adrenergic receptors [2]
Clinically, it is suitable for emergency treatment of allergic reactions, cardiac arrest, acute exacerbations of bronchial asthma, and acute hypotension [1]
Due to poor oral absorption and short half-life, it is usually administered intravenously, subcutaneously, or intramuscularly for rapid onset of action [1]

C9H13NO3.HCL

219.67

219.066

C, 49.21; H, 6.42; Cl, 16.14; N, 6.38; O, 21.85

55-31-2

441411

Solid powder

413.1ºC at 760 mmHg

157°C

207.9ºC

1.543

5

4

3

14

154

1

CNC[C@@H](C1=CC(=C(C=C1)O)O)O.Cl

ATADHKWKHYVBTJ-FVGYRXGTSA-N

InChI=1S/C9H13NO3.ClH/c1-10-5-9(13)6-2-3-7(11)8(12)4-6;/h2-4,9-13H,5H2,1H3;1H/t9-;/m0./s1

4-[(1R)-1-hydroxy-2-(methylamino)ethyl]benzene-1,2-diol;hydrochloride

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)

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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