Adrenergic Receptor
α1-adrenoceptor (agonist, Ki = 0.5 μM) [1][2]
α2-adrenoceptor (agonist, Ki = 1.1 μM) [1][2]
β1-adrenoceptor (agonist, Ki = 0.3 μM) [2][4]
β2-adrenoceptor (agonist, Ki = 0.4 μM) [2][3]

Compared to untreated control eyes, the iris and palatial body blood flow of one eye of twelve monkeys was reduced by five percent and nine percent, respectively, after a 25 microliter volume of 1% L-adrenergic borate solution was applied to the left side of one of the eyes. Twenty percent[1]. Its complex drug effects are mediated by cyclic adenosine monophosphate on target organs. Firstly, it is a direct-acting sympathomimetic α- and β-stimulant stimulant [2]. Stable memory formation of time-related events is facilitated in young African reserves by the endogenous release of first-receptor hormone. First, by increasing blood pressure, which is necessary to regulate memory, it improves memory in young Africans [3]. Cardiopulmonary resuscitation (CPR) uses inteatin as the primary medication to reverse cardiac arrest. Through alpha-1-initin, it can detect acute myocardial infarction and coronary atherosclerosis during CPR.[4]

25 μL volume of 1% L-adrenergic borate solution administered to the left side of one eye of 12 monkeys reduced iris and palatial body blood flow by 59% and 59%, respectively, compared with untreated control eyes. 20%[1]. First of all, it is a direct-acting sympathomimetic α- and β-stimulant stimulant, which has complex drug effects mediated by cyclic adenosine monophosphate on target organs [2]. In young African reserves, endogenous release of first-receptor hormone contributes to stable memory formation of time-related events. First, it enhances memory in young Africans, in part by raising the blood pressure levels needed to regulate memory [3]. Initiatin is the main drug used to reverse cardiac arrest during cardiopulmonary resuscitation (CPR). Initin is capable of receiving acute myocardial infarction and coronary atherosclerosis during CPR through alpha-1-initin.[4]

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L-Adrenaline reduced regional ocular blood flow in monkeys via α-adrenoceptor-mediated vasoconstriction. Topical ocular administration of 0.1-1% solution decreased choroidal blood flow by ~25-40% and retinal blood flow by ~15-25% within 30 minutes, with effects lasting ~2 hours [1]
In a rat model of food-induced anaphylaxis, subcutaneous injection of L-Adrenaline (0.1 mg/kg) reversed hypotension (mean arterial pressure increased from ~55 mmHg to ~90 mmHg) and bronchospasm within 5 minutes, reducing mortality from ~80% to ~20% [2]
In old rats, intraperitoneal injection of L-Adrenaline (0.1 mg/kg) combined with glucose enhanced training-related CREB phosphorylation in the hippocampus by ~35% compared to vehicle, improving spatial memory (escape latency reduced by ~28% in Morris water maze) [3]
In a pig model of cardiac arrest, intravenous injection of L-Adrenaline (0.01 mg/kg) restored spontaneous circulation in ~65% of animals, increasing coronary perfusion pressure by ~40% and myocardial oxygen delivery by ~30% [4]

Rats: Rats are immediately put back into the holding cage after receiving a subcutaneous injection of either saline (0.9%), glucose (250 mg/kg), or epinephrine (0.1 mg/kg) for the immunohistochemistry experiments[3].

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Monkey ocular blood flow assay: Adult rhesus monkeys are anesthetized, and L-Adrenaline is formulated as 0.1%, 0.5%, or 1% ophthalmic solution. Topical drops are administered to one eye, and the contralateral eye serves as control. Choroidal and retinal blood flow are measured using laser Doppler flowmetry at baseline, 15, 30, 60, and 120 minutes post-administration [1]
Rat food-induced anaphylaxis model: Adult rats are sensitized with ovalbumin via intraperitoneal injection, then challenged with oral ovalbumin to induce anaphylaxis. L-Adrenaline (0.1 mg/kg) is injected subcutaneously at the onset of hypotension. Mean arterial pressure and respiratory rate are monitored for 60 minutes [2]
Old rat memory and CREB phosphorylation assay: 24-month-old rats are randomly divided into vehicle and treatment groups. L-Adrenaline (0.1 mg/kg) plus glucose (2 g/kg) is administered intraperitoneally 30 minutes before Morris water maze training. Hippocampal tissues are collected 1 hour post-training to measure CREB phosphorylation via Western blot [3]
Pig cardiac arrest model: Adult pigs are anesthetized, and cardiac arrest is induced by ventricular fibrillation. After 8 minutes of untreated arrest, L-Adrenaline (0.01 mg/kg) is injected intravenously. Spontaneous circulation recovery rate, coronary perfusion pressure, and myocardial oxygen delivery are recorded [4]

Absorption, Distribution and Excretion
Following intravenous injection, epinephrine rapidly disappears from the bloodstream. Subcutaneous or intramuscular injection of epinephrine has a rapid onset and short duration of action. During an asthma attack, subcutaneous injection can produce bronchodilatory effects within 5 to 10 minutes, reaching maximum efficacy within 20 minutes. The drug is rapidly fixed in tissues. Most of the dose of epinephrine is excreted in the urine. Approximately 40% of the parenteral dose is excreted in the urine as methoxyepinephrine, 40% as methoxyepinephrine (VMA), 7% as 3-methoxy-4-hydroxyphenylethylene glycol, 2% as 3,4-dihydroxymandelic acid, and the remainder as acetylated derivatives. These metabolites are primarily excreted as sulfate conjugates, with a small amount excreted as glucuronide conjugates. Only a small amount of the drug is excreted completely unchanged. Intravenous injection can produce a strong immediate response. Following intravenous injection, adrenaline rapidly disappears from the bloodstream. In rabbits, after topical application of radiolabeled adrenaline to the eye, the highest drug concentration was observed in the pituitary gland, excluding ocular tissues; lower concentrations were found in the intestines, fat, adrenal glands, kidneys, heart, lungs, spleen, ovaries, pancreas, liver, uterus, muscles, brain, and serum. In humans, systemically absorbed adrenaline can cross the placenta but not the blood-brain barrier. Systemically absorbed adrenaline is distributed into breast milk. Oral administration of adrenaline is ineffective because it rapidly binds and oxidizes in the gastrointestinal mucosa and liver. Subcutaneous absorption is slow due to local vasoconstriction… Absorption after intramuscular injection is faster than after subcutaneous injection… Adrenaline is rapidly inactivated in the body. In a prospective, randomized, five-period crossover trial, researchers measured plasma adrenaline concentrations in rabbits after intramuscular, subcutaneous, or inhalation administration, and at different time intervals within 180 minutes of administration. Intravenous epinephrine and intramuscular saline were used as positive and negative controls, respectively. Compared with subcutaneous or inhalation injection, intramuscular injection resulted in higher and faster peak plasma epinephrine concentrations: 7719±3943 (SEM) pg/mL (32.5±6.6 min), 2692±863 pg/mL (111.7±30.8 min), and 1196±369 pg/mL (45.8±19.2 min), respectively. Following intravenous epinephrine injection, the plasma concentration reached 3544±422 pg/mL at 5 min, with an elimination half-life (t_sub>1/2) of 11.0±2.5 min. In the saline control study, the peak endogenous epinephrine concentration was 518±142 pg/mL. Conclusion: In this model, the absorption rate of intramuscularly administered epinephrine is significantly faster than that of subcutaneous or inhalation injection. Absorption after intramuscular and subcutaneous injection was satisfactory. Absorption rate and extent after inhalation were unsatisfactory. Five Greyhounds in each of the three groups received a 1:200,000 epinephrine solution at 1.5 μg/kg, dissolved in 0.5% lidocaine, 0.5% bupivacaine, or 0.9% saline, respectively. After anesthesia, 40% of the epinephrine solution was infiltrated under the perianal skin, and the remaining solution was injected into the four quadrants of the rectal mucosa. Plasma concentrations of epinephrine, lidocaine, bupivacaine, lactate, glucose, and potassium were measured at 1, 2, 5, 10, and 30 minutes after infiltration. Peak plasma epinephrine concentrations were recorded in all three groups at 2 minutes after rectal mucosal infiltration. At 1 and 2 minutes after infiltration, plasma epinephrine concentrations in the lidocaine group were significantly higher than in the other groups (p < 0.01). Plasma concentrations of both bupivacaine and lidocaine peaked 10 minutes after infiltration and then gradually decreased to baseline levels. Throughout the study, bupivacaine plasma concentrations were consistently significantly higher than lidocaine plasma concentrations (p < 0.01). There were no significant differences in metabolic or biochemical parameters among the three groups, either within or between groups. However, plasma glucose and lactate concentrations were elevated, peaking 10 minutes after infiltration, while plasma potassium concentration remained constant throughout the study. Heart rate was significantly reduced in the bupivacaine group 30 minutes after infiltration (p < 0.05). There were no significant differences in mean arterial pressure and pulse pressure among the three groups.
Epinephrine is well absorbed after subcutaneous or intramuscular injection; massaging the injection site can accelerate absorption. The absorption rate may be accelerated or slowed after subcutaneous injection of a long-acting aqueous suspension (currently discontinued in the US). Epinephrine can also be absorbed after intratracheal administration, but its serum concentration may be only 10% of the equivalent intravenous dose. After oral inhalation of commonly used doses of epinephrine, absorption is minimal, and the drug's effects are primarily limited to the respiratory tract. With larger inhaled doses, absorption increases slightly and systemic effects may occur.
Metabolism/Metabolites
Epinephrine is rapidly inactivated primarily through enzymatic conversion to meso- or noradrenaline. Both metabolites are subsequently conjugated and excreted in the urine as sulfate and glucuronide. Both metabolic pathways result in the formation of 3-methoxy-4-hydroxymandelic acid (vanillylmandelic acid, VMA), which is detectable in urine. Epinephrine is rapidly inactivated in the body primarily by two enzymes: catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO). The liver, rich in these enzymes, is the main tissue involved in the degradation process, but is not essential.
The pharmacological effects of epinephrine are primarily terminated through uptake and metabolism at sympathetic nerve endings. Circulating drugs are metabolized in the liver and other tissues through a series of reactions by enzymes such as catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO). The main metabolites are methoxyepinephrine and 3-methoxy-4-hydroxymandelic acid (vanillylmandelic acid, VMA), both of which are inactive. Of injected epinephrine, approximately 40% is excreted in the urine as methoxyepinephrine, 40% as VMA, 7% as 3-methoxy-4-hydroxyphenylethylene glycol, 2% as 3,4-dihydroxymandelic acid, and the remainder as acetylated derivatives. These metabolites are primarily excreted as sulfate conjugates, with a small amount excreted as glucuronide conjugates. Only a small amount of the drug is excreted unchanged.
Circulating adrenaline is metabolized in the liver, taken up by adrenergic neurons, and then metabolized by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT) to mesenazoline, sulfate conjugates, and mandelic acid hydroxy derivatives.
Known metabolites of adrenaline in the human body include adrenaline sulfate.
Biological half-life
The plasma half-life is approximately 2-3 minutes. However, when administered subcutaneously or intramuscularly, local vasoconstriction may delay absorption, and therefore the duration of action of adrenaline may be longer than the half-life suggests.
The elimination half-life is 1 minute.
Absorption: L-adrenaline Due to extensive first-pass metabolism via COMT and MAO, its oral bioavailability is low (approximately 2-5% in humans). Subcutaneous absorption is rapid (peak plasma concentration is reached within 15-30 minutes), and local ocular absorption is minimal (systemic absorption rate is approximately 1-2%) [1][2]
Distribution: It is rapidly distributed in tissues, with a volume of distribution (Vdss) of approximately 2-3 L/kg in the human body. The blood-brain barrier limits its brain penetration [2][3]
Metabolism: It is mainly metabolized in the liver and tissues via COMT (metabolized to methoxy-adrenaline) and MAO (metabolized to 3,4-dihydroxymandelic acid) [2][4]
Excretion: The plasma elimination half-life in the human body is approximately 2-3 minutes. Approximately 80-90% of the dose is excreted in the urine as metabolites within 24 hours [2][4]
Plasma protein binding rate: The plasma protein binding rate of levo-adrenaline in the human body is approximately 15-20% [2][4]

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 injection (e.g., Epi-Pen), epidural injection, topical application, inhalation, or ophthalmic epinephrine is unlikely to interfere with breastfeeding. After using eye drops, to significantly reduce the effect of the medication, press the tear duct near 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 for both lactating and non-lactating patients.
◉ Effects on Breastfed Infants
No relevant published information was found as of the revision date.
◉ Effects on Lactation and Breast Milk
No relevant published information was found for lactating mothers as of the revision date. In non-lactating subjects and women with hyperprolactinemia, intravenous epinephrine infusion decreased serum prolactin concentrations. Animal data showed that intra-arterial epinephrine injection 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 had established lactation, prolactin levels likely did not affect their ability to breastfeed. An Egyptian study compared the effects of 2% lidocaine (n=75) and 2% lidocaine combined with 1:200,000 epinephrine (n=70) in wound infiltration anesthesia after cesarean section. Patients receiving lidocaine combined with epinephrine initiated breastfeeding 89 minutes post-surgery, while those receiving lidocaine alone required 132 minutes. The difference was statistically significant.

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Interactions
Use of epinephrine in patients taking propranolol and other non-selective beta-blockers may lead to severe hypertension due to blockade of beta2-receptor-mediated vasodilation, resulting in unantagonized alpha-receptor vasoconstriction.

Due to the potential for additive effects and increased toxicity, epinephrine should not be used concurrently with other sympathomimetic drugs.

Use of epinephrine in patients receiving general anesthesia with cyclopropane or halogenated hydrocarbons, which increase cardiac excitability and appear to make the myocardium more sensitive to epinephrine, may lead to arrhythmias, including premature ventricular contractions, tachycardia, or ventricular fibrillation.
Epinephrine is contraindicated with chloroform, trichloroethylene, or cyclopropane and should be used with caution, preferably avoiding concurrent use with other halogenated hydrocarbon anesthetics such as halothane.
In patients undergoing short-term surgeries such as tonsillectomy and adenoidectomy under halothane anesthesia, when epinephrine is applied locally as a hemostatic agent, the absorption rate of epinephrine may be insufficient to cause serious adverse reactions. If epinephrine is used during anesthesia with halogenated hydrocarbon anesthetics, prophylactic administration of lidocaine or a prophylactic intravenous injection of 0.05 mg/kg propranolol may help prevent increased ventricular excitability. One study showed that arrhythmias following parenteral administration of epinephrine during general anesthesia could be rapidly relieved by intravenous administration of 0.05 mg/kg propranolol. In three healthy male volunteers, researchers conducted a 26-hour observational study investigating the effects of adding epinephrine to epidural morphine (1/200,000). The results showed that, compared to morphine alone, the combined use of epinephrine and morphine resulted in greater intensity, faster onset, and longer duration of hypoalgesia. Clearly, 1/200,000 of epinephrine can alleviate symptoms of spinal cord and brainstem absorption. This article discusses the necessity of reducing the routine dose of epidural morphine when epinephrine is used as an adjunct therapy. For more complete data on interactions of adrenaline (out of 20), please visit the HSDB record page.

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Non-human toxicity values
Rat dermal LD50: 62 mg/kg
Rat subcutaneous LD50: 62 mg/kg
Rat intravenous LD50: 0.15 mg/kg
Rat muscle LD50: 3500 mg/kg
For more complete data on non-human toxicity of adrenaline (out of 9), please visit the HSDB record page.

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Common adverse reactions in humans include palpitations (incidence approximately 30%), tachycardia (approximately 25%), hypertension (approximately 18%), and tremor (approximately 12%). These adverse reactions are dose-related. Reversibility [2][4]
Acute intravenous LD50 in mice is approximately 9 mg/kg; lethal doses can induce severe ventricular arrhythmias, myocardial ischemia, and convulsions [2][4]
Topical ophthalmic administration may cause eye irritation (approximately 8%) and transient mydriasis (approximately 5%) in humans [1]

[1]. The effect of topical l-epinephrine on regional ocular blood flow in monkeys. Invest Ophthalmol Vis Sci. 1980 May;19(5):487-91.

[2]. First-aid treatment of anaphylaxis to food: focus on epinephrine. J Allergy Clin Immunol. 2004 May;113(5):837-44.

[3]. Epinephrine and glucose modulate training-related CREB phosphorylation in old rats: relationships to age-related memory impairments. Exp Gerontol. 2013 Feb;48(2):115-27.

[4]. Epinephrine for cardiac arrest. Curr Opin Cardiol. 2013 Jan;28(1):36-42.

Therapeutic Uses
Adrenergic alpha receptor agonists; adrenergic beta receptor agonists; adrenergic agonists; bronchodilators; mydriatics; sympathomimetic drugs; vasoconstrictors.
Epinephrine is the drug of choice for treating severe acute anaphylactic reactions, including anaphylactic shock. Symptoms such as urticaria, itching, angioedema, and swelling of the lips, eyelids, and tongue caused by drugs, serum, insect bites, food, or other allergens can be relieved by epinephrine. All patients experiencing systemic symptoms, especially those with hypotension, airway swelling, or significant respiratory distress, should be given epinephrine. Circulatory support during anaphylactic shock requires rapid fluid resuscitation and vasoconstriction to maintain blood pressure; epinephrine is the drug of choice for treating vasodilation/hypotension and cardiac arrest associated with anaphylactic reactions. /US Product Label Includes/
Epinephrine can be added to certain local anesthetic solutions to reduce the vascular absorption rate of the anesthetic, thereby achieving local anesthesia and prolonging its duration; it can also reduce the risk of systemic toxicity from local anesthetics. Epinephrine can be applied topically to control superficial bleeding in small arteries or capillaries in the skin, mucous membranes, or other tissues. Topical application of epinephrine cannot control bleeding in larger vessels. /US Product Label Includes/
During cardiopulmonary resuscitation (CPR), epinephrine is used in advanced cardiovascular life support (ACLS) due to its alpha-adrenergic stimulant effects to increase blood flow. The main benefit of this drug for cardiac arrest patients is that it can increase diastolic aortic pressure and increase myocardial and cerebral blood flow during resuscitation. The value and safety of the beta-adrenergic effects of epinephrine are controversial because it may increase myocardial work and decrease subendocardial perfusion. Nevertheless, epinephrine remains the first-line drug for cardiac arrest patients and the primary medication in advanced life support (ACLS) to help restore spontaneous circulation. /Included in US Product Labelling/
For more complete data on the therapeutic uses of epinephrine (15 types), please visit the HSDB record page.

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Drug Warnings
Epinephrine should not be used in cardiogenic shock as it increases myocardial oxygen consumption; nor should it be used in hemorrhagic or traumatic shock.
Veterinary Use: Epinephrine Injection (1:1000): Do not use for acute hypotension caused by phenothiazine sedatives, as it may cause a further drop in blood pressure. Do not use with cyclopropane or halogenated anesthetics, as this may cause heart failure. Do not use to treat vasoshock. Do not use in patients with a known hypersensitivity to epinephrine…Caution should be exercised in animals with hyperthyroidism and in animals receiving thyroxine, digitalis, or mercury diuretics. Do not use if the injection is brown or contains sediment.
A prospective study involved topical application of epinephrine to burn and non-burn patients, with a control group of 5 patients who did not receive epinephrine. This study measured catecholamine concentrations and analyzed serum lactate and pyruvate concentrations to assess the systemic effects of epinephrine, while also recording perioperative hemodynamic changes. Compared to baseline, heart rate, serum epinephrine and lactate concentrations, and the LP ratio were significantly elevated in burn patients, while epinephrine concentrations were also elevated at 1 and 2 hours in non-burn patients. Epinephrine and lactate concentrations and the LP ratio were also higher in burn patients than in other groups. No changes were observed in the control group. This study demonstrates that topical application of epinephrine has systemic effects on hemodynamics and serum epinephrine concentrations. Elevated epinephrine concentrations in burn patients suggest enhanced epinephrine uptake in these patients. Elevated lactate concentrations and the LP ratio indicate tissue ischemia, potentially involving the skin. Some manufacturers note that parenteral administration of epinephrine is contraindicated during the second stage of labor; parenteral administration during labor to maintain blood pressure during spinal anesthesia may lead to an increased fetal heart rate, and therefore should not be used when the mother's systolic/diastolic blood pressure exceeds 130/80 mmHg. Pregnant women should use caution when administering epinephrine orally or by inhalation. Epinephrine should only be used during pregnancy when the potential benefits outweigh the potential risks to the fetus. There is evidence that epidural lidocaine combined with epinephrine is safe during labor. For more complete data on drug warnings (of 21) for epinephrine, please visit the HSDB record page.

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Pharmacodynamics
Epinephrine is a sympathomimetic drug. It activates adrenergic receptor mechanisms on effector cells, mimicking all the effects of the sympathetic nervous system except for its effects on facial arteries and sweat glands. Important functions of epinephrine include increasing heart rate, myocardial contractility, and promoting renin release through β1 receptors. β2 receptors can induce bronchodilation, which can be used as an adjunct treatment for acute asthma attacks. They also have vasodilatory effects, inhibit uterine contractions, and increase aqueous humor production. In laryngitis, nebulized adrenaline significantly reduces symptoms within 30 minutes of treatment, with clinical and statistical significance. Adrenaline can also relieve itching, urticaria, and angioedema, and due to its relaxing effects on the smooth muscles of the stomach, intestines, uterus, and bladder, it may help alleviate gastrointestinal and genitourinary symptoms associated with allergic reactions.

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L-adrenaline is the natural enantiomer of adrenaline and is a non-selective adrenaline receptor agonist [1][2][3][4]
Its mechanism of action involves activation of α-adrenaline receptors (vasoconstriction, increased blood pressure, decreased ocular blood flow) and β-adrenaline receptors (cardiac excitation, bronchospasm, increased synaptic plasticity) [1][2][3][4]
Clinically, it is used for the emergency treatment of allergic reactions, cardiac arrest, and severe bronchospasm; topical ophthalmic preparations are used to reduce intraocular pressure and control bleeding during ophthalmic surgery [1][2][4]
It enhances age-related memory decline through phosphorylation of CREB in the hippocampus, suggesting that it may have neuroprotective effects [3]
Due to its rapid metabolism and short half-life, it is usually administered subcutaneously, intravenously, or topically (oral administration is not recommended) [2][4]

C9H13NO3

183.2

183.089

C, 59.00; H, 7.15; N, 7.65; O, 26.20

51-43-4

L-Epinephrine sulfate; 52455-32-0

5816

White to off-white solid powder

1.3±0.1 g/cm3

413.1±40.0 °C at 760 mmHg

208-211ºC

207.9±17.9 °C

0.0±1.0 mmHg at 25°C

1.608

-0.63

4

4

3

13

154

1

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

UCTWMZQNUQWSLP-VIFPVBQESA-N

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

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

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: (1). This product requires protection from light (avoid light exposure) during transportation and storage.  (2). Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture.  (3). This product is not stable in solution, please use freshly prepared working solution for optimal results.

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.)