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Methyldopa (MK-351)

Alias: Dopamet; Dopegit; Dopegyt; Dopergit; Hydopa; Meldopa; Nu-Medopa; Nu Medopa; NuMedopa; Methyldopa; MK-351; MK 351
Cat No.:V1135 Purity: ≥98%
Methyldopa (marketed under the brand names Aldomet; Dopamet; Dopegyt; Dopergit; Hydopa; Meldopa; Nu-Medopa; MK-351; MK 351), the methylated form of Dopa, is a potent andcompetitiveDOPA decarboxylase inhibitor with antihypertensive effects.
Methyldopa (MK-351)
Methyldopa (MK-351) Chemical Structure CAS No.: 555-30-6
Product category: Adrenergic Receptor
This product is for research use only, not for human use. We do not sell to patients.
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Other Forms of Methyldopa (MK-351):

  • Methyldopa Sesquihydrate
  • L-(-)-α-Methyldopa hydrochloride
Official Supplier of:
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Purity & Quality Control Documentation

Purity: ≥98%

Product Description

Methyldopa (marketed under the brand names Aldomet; Dopamet; Dopegyt; Dopergit; Hydopa; Meldopa; Nu-Medopa; MK-351; MK 351), the methylated form of Dopa, is a potent and competitive DOPA decarboxylase inhibitor with antihypertensive effects. It suppresses the enzyme dogaclase with an ED50 of 21.8 mg/kg. Methyldopa is a drug used to treat hypertension. It is one of the recommended therapies for pregnancy-related hypertension. Other medications are usually preferred for other types of high blood pressure, such as extremely high blood pressure that causes symptoms. It can be administered intravenously or orally. The effects take about five hours to start and last for about a day.

Biological Activity I Assay Protocols (From Reference)
Targets
α adrenergic receptor
ln Vivo
Methyldopa (L-(-)-α-Methyldopa; 200 mg/kg; i.p.) reduces the hyperglycemic reaction during the initial two hours following Dieldrin administration[2].
Animal Protocol
60-day-old male rats
200 mg/kg
I.p.
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
Methyldopa is incompletely absorbed from the gastrointestinal tract following oral administration. In healthy individuals, the inactive D-isomer is less readily absorbed than the active L-isomer. The mean bioavailability of methyldopa is 25%, ranging from eight to 62%. Following oral administration, about 50% of the dose is absorbed and Tmax is about three to six hours.
Approximately 70% of absorbed methyldopa is excreted in the urine as unchanged parent drug (24%) and α-methyldopa mono-O-sulfate (64%), with variability.3-O-methyl-α-methyldopa accounted for about 4% of urinary excretion products. Other metabolites like 3,4-dihydroxyphenylacetone, α-methyldopamine, and 3-O-methyl-α-methyldopamine are also excreted in urine. Unabsorbed drug is excreted in feces as the unchanged parent compound. After oral doses, excretion is essentially complete in 36 hours. Due to attenuated excretion in patients with renal failure, accumulation of the drug and its metabolites may occur, possibly leading to more profound and prolonged hypotensive effects in these patients.
The apparent volume of distribution ranges between 0.19 and 0.32L/kg and the total volume of distribution ranges from 0.41 to 0.72L/kg. Since methyldopa is lipid-soluble, it crosses the placental barrier, appears in cord blood, and appears in breast milk.
The renal clearance is about 130 mL/min in normal subjects and is decreased in patients with renal insufficiency.
(14)C-METHYLDOPA ADMIN ORALLY TO HYPERTENSIVE PT IS RECOVERED EQUALLY FROM URINE & FECES; PRODUCT IN FECES IS UNCHANGED METHYLDOPA, & IN URINE METHYLDOPA & ITS ETHEREAL SULFATE, TOGETHER WITH SMALL AMT OF 3-O-METHYL-METHYLDOPA & METHYLDOPAMINE.
METHYLDOPA CROSSES THE PLACENTA...
Methyldopa is partially absorbed from the GI tract. The degree of absorption varies among individuals and in the same patient from day to day, but generally about 50% of an oral dose is absorbed.
Metabolism / Metabolites
Two isomers of methyldopa undergo different metabolic pathways. L-α-methyldopa is biotransformed to its pharmacologically active metabolite, alpha-methylnorepinephrine. Methyldopa is extensively metabolized in the liver to form the main circulating metabolite in the plasma, alpha (α)-methyldopa mono-O-sulfate. Its other metabolites also include 3-O-methyl-α-methyldopa; 3,4-dihydroxyphenylacetone; α-methyldopamine; and 3-O-methyl-α-methyldopamine. These metabolites are further conjugated in the liver to form sulfate conjugates. After intravenous administration, the most prominent metabolites are alpha-methyldopamine and the glucuronide of dihydroxyphenylacetone, along with other uncharacterized metabolites. D-α-methyldopa, which is the inactive isomer of methyldopa, is also metabolized to 3-O-methyl-α-methyldopa and 3,4-dihydroxyphenylacetone to a minimal extent; however, there are no amines (α-methyldopamine and 3-O-methyl-α-methyldopamine) formed.
METHYLDOPA YIELDS 3,4-DIHYDROXY-ALPHA-METHYLPHENETHYLAMINE, 3,4-DIHYDROXY-ALPHA-METHYL-L-PHENYLALANINE-O-SULFATE, & 4-HYDROXY-3-METHOXY-ALPHA-METHYL-L-PHENYLALANINE IN MAN. /FROM TABLE/
METHYLDOPA...UNDERGOES DECARBOXYLATION & BETA-HYDROXYLATION IN MOUSE & RABBIT BRAIN TO YIELD ALPHA-METHYLNORADRENALINE.
...ADMIN IP TO RATS (14)C-METHYLDOPA IS EXCRETED IN URINE AS...3-O-METHYL-METHYLDOPA (14%), METHYLDOPAMINE & ITS CONJUGATES (2%), 3-O-METHYL-METHYLDOPAMINE & ITS CONJUGATES (6%), 3-METHOXY-4-HYDROXYPHENYLACETONE (6%), & 3,4-DIHYDROXYPHENYLACETONE (10%).
A REVIEW ON THE METAB OF ALPHA-METHYLDOPA.
Hepatic, extensively metabolized. The known urinary metabolites are: a-methyldopa mono-0-sulfate; 3-0-methyl-a-methyldopa; 3,4-dihydroxyphenylacetone; a-methyldopamine; 3-0-methyl-a-methyldopamine and their conjugates.
Route of Elimination: Methyldopa is extensively metabolized. The known urinary metabolites are: alpha-methyldopa mono-O-sulfate; 3-0-methyl-alpha-methyldopa; 3,4-dihydroxyphenylacetone; alpha-methyldopamine; 3-0-methyl-alpha-methyldopamine and their conjugates. Approximately 70 percent of the drug which is absorbed is excreted in the urine as methyldopa and its mono-O-sulfate conjugate. Methyldopa crosses the placental barrier, appears in cord blood, and appears in breast milk.
Half Life: The plasma half-life of methyldopa is 105 minutes.
Biological Half-Life
The plasma half-life of methyldopa is 105 minutes. Following intravenous injection, the plasma half-life of methyldopa ranges from 90 to 127 minutes.
The drug is ... eliminated with a half-life of about 2 hr. ... The half-life of methyldopa is prolonged to 4-6 hr in patients with renal failure.
DISAPPEARANCE OF THE DRUG FROM PLASMA AFTER IV ADMIN IS BIPHASIC, & THE TERMINAL HALF-TIME OF ELIMINATION FROM PLASMA IS ABOUT 2 HOURS. RENAL EXCRETION ACCOUNTS FOR ABOUT TWO THIRDS OF THE CLEARANCE OF DRUG FROM PLASMA.
IN PT WITH SEVERELY IMPAIRED RENAL FUNCTION, ONLY ABOUT 50% OF DRUG IS EXCRETED DURING EARLY PHASE (T/2= 3 1/2 HR), & SOME ACCUMULATION CAN OCCUR DURING CHRONIC ADMIN... BOTH TOTAL QUANTITY ABSORBED & DISTRIBUTION OF METABOLITES IN URINE CAN VARY CONSIDERABLY IN DIFFERENT INDIVIDUALS & IN SAME PT FROM DAY TO DAY.
Toxicity/Toxicokinetics
Hepatotoxicity
Drug induced liver injury due to methyldopa was identified shortly after its introduction into medical use in the 1960’s. Chronic use of methyldopa is associated with mild and transient elevations in serum aminotransferase levels in 5% to 35% of patients, these elevations often resolving despite continuation of the medication. In contrast, clinically apparent or significant liver injury from methyldopa is relatively uncommon, although several hundred cases have been reported. Two patterns of hepatotoxicity have been described: an acute hepatitis that appears within weeks to months of starting treatment, and a chronic hepatitis that arises months to years after initiation of methyldopa therapy.
The acute liver injury from methyldopa generally arises within 2 to 12 weeks of starting therapy and is typically hepatocellular with marked elevations in ALT and AST (5- to 100-fold) and modest increases in alkaline phosphatase, although in a small proportion of patients the pattern of enzyme elevations is mixed or cholestatic (Case 1 and 2). Most patients become jaundiced. Symptoms resemble those of acute viral hepatitis, including fever, headache, fatigue, anorexia and nausea. Signs of hypersensitivity other than fever are uncommon. The injury can be severe and fatal. While some cases are associated with marked cholestasis and prolonged jaundice, most patients recover within 4 to 12 weeks. Autoantibodies including Coombs and antinuclear antibody positivity may be present (but also can arise independent of liver injury). Liver biopsy shows an acute hepatitis-like picture with marked inflammatory infiltrates and fatty change, with variable amounts of necrosis. Rechallenge leads to rapid recurrence of liver injury and can result in severe hepatitis, acute liver failure and death.
The chronic liver injury from methyldopa usually arises after 6 months, but may become first evident after several years of therapy (Case 3). This chronic hepatitis-like clinical picture has a more insidious onset typically with fatigue, weakness and nausea associated with mild or no jaundice. Clinical features may include liver enlargement and tenderness and spider angiomata. The clinical and laboratory pattern often resembles autoimmune hepatitis, with moderate to marked elevations in ALT and AST, modest alkaline phosphatase elevations, increases in immunoglobulin levels (particularly IgG), and high titers of autoantibodies such as antinuclear antibody (ANA) and smooth muscle antibody (SMA). Liver biopsy demonstrates findings of chronic active hepatitis with variable amounts of fatty change and fibrosis. Plasma cell infiltrates may be prominent. Cirrhosis and end stage liver disease can occur if the drug is continued. The disease resolves slowly but completely with discontinuation of methyldopa. Chronic liver injury now appears to be the most common form of drug induced liver injury from this agent. Some cases of methyldopa induced liver injury have features of both acute and chronic injury and the two forms of hepatic injury may share a common etiology.
African Americans appear to have a higher risk for liver injury from methyldopa than Caucasians or Hispanic individuals. The course may be more severe and outcome less favorable in Africans Americans as well. Granulomatous hepatitis can also occur with methyldopa therapy, usually in association with drug fever and systemic symptoms (and granulomas elsewhere), and sometimes with granulomatous myocarditis which can be fatal. In these situations, the liver injury is usually mild and anicteric.
Likelihood score: A (well known cause of clinically apparent liver injury).
Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Because of the low levels of methyldopa in breastmilk, amounts ingested by the infant are small and would not be expected to cause any adverse effects in breastfed infants. No special precautions are required.
◉ Effects in Breastfed Infants
No acute or long-term adverse effects were reported in any 15 infants ranging in age from less than 1 week to 8 weeks of age whose mothers were taking oral methyldopa 0.25 to 1.5 grams daily.
◉ Effects on Lactation and Breastmilk
Methyldopa can increase serum prolactin and has caused galactorrhea. The maternal prolactin level in a mother with established lactation may not affect her ability to breastfeed.
Protein Binding
Methyldopa is less than 15% bound to plasma proteins and its primary metabolite, O-sulfate metabolite, is about 50% protein bound. Following intravenous administration, approximately 17% of the dose in normal subjects were circulating in the plasma as free methyldopa.
References

[1]. New centrally acting antihypertensive drugs related to methyldopa and clonidine. Hypertension. 1984;6(5 Pt 2):II51-II56.

[2]. The effects of phenobarbital, atropine, L-alpha-methyldopa, and DL-propranolol on dieldrin-induced hyperglycemia in the adult rat. Toxicol Appl Pharmacol. 1985;78(3):342-350.

Additional Infomation
Methyl dopa appears as colorless or almost colorless crystals or white to yellowish-white fine powder. Almost tasteless. In the sesquihydrate form. pH (saturated aqueous solution) about 5.0. (NTP, 1992)
Alpha-methyl-L-dopa is a derivative of L-tyrosine having a methyl group at the alpha-position and an additional hydroxy group at the 3-position on the phenyl ring. It has a role as a hapten, an antihypertensive agent, an alpha-adrenergic agonist, a peripheral nervous system drug and a sympatholytic agent. It is a L-tyrosine derivative and a non-proteinogenic L-alpha-amino acid.
Methyldopa, or α-methyldopa, is a centrally acting sympatholytic agent and an antihypertensive agent. It is an analog of DOPA (3,4‐hydroxyphenylanine), and it is a prodrug, meaning that the drug requires biotransformation to an active metabolite for therapeutic effects. Methyldopa works by binding to alpha(α)-2 adrenergic receptors as an agonist, leading to the inhibition of adrenergic neuronal outflow and reduction of vasoconstrictor adrenergic signals. Methyldopa exists in two isomers D-α-methyldopa and L-α-methyldopa, which is the active form. First introduced in 1960 as an antihypertensive agent, methyldopa was considered to be useful in certain patient populations, such as pregnant women and patients with renal insufficiency. Since then, methyldopa was largely replaced by newer, better-tolerated antihypertensive agents; however, it is still used as monotherapy or in combination with [hydrochlorothiazide]. Methyldopa is also available as intravenous injection, which is used to manage hypertension when oral therapy is unfeasible and to treat hypertensive crisis.
Methyldopa anhydrous is a Central alpha-2 Adrenergic Agonist. The mechanism of action of methyldopa anhydrous is as an Adrenergic alpha2-Agonist.
Methyldopa (alpha-methyldopa or α-methyldopa) is a centrally active sympatholytic agent that has been used for more than 50 years for the treatment of hypertension. Methyldopa has been clearly linked to instances of acute and chronic liver injury that can be severe and even fatal.
Methyldopa is a phenylalanine derivative and an aromatic amino acid decarboxylase inhibitor with antihypertensive activity. Methyldopa is a prodrug and is metabolized in the central nervous system. The antihypertensive action of methyldopa seems to be attributable to its conversion into alpha-methylnorepinephrine, which is a potent alpha-2 adrenergic agonist that binds to and stimulates potent central inhibitory alpha-2 adrenergic receptors. This results in a decrease in sympathetic outflow and decreased blood pressure.
Methyldopa or alpha-methyldopa (brand names Aldomet, Apo-Methyldopa, Dopamet, Novomedopa) is a centrally-acting adrenergic antihypertensive medication. Its use is now deprecated following introduction of alternative safer classes of agents. However it continues to have a role in otherwise difficult to treat hypertension and gestational hypertension (formerly known as pregnancy-induced hypertension). Methyldopa is an aromatic-amino-acid decarboxylase inhibitor in animals and in man. Only methyldopa, the L-isomer of alpha-methyldopa, has the ability to inhibit dopa decarboxylase and to deplete animal tissues of norepinephrine. In man the antihypertensive activity appears to be due solely to the L-isomer. About twice the dose of the racemate (DL-alpha-methyldopa) is required for equal antihypertensive effect. Methyldopa has no direct effect on cardiac function and usually does not reduce glomerular filtration rate, renal blood flow, or filtration fraction. Cardiac output usually is maintained without cardiac acceleration. In some patients the heart rate is slowed. Normal or elevated plasma renin activity may decrease in the course of methyldopa therapy. Methyldopa reduces both supine and standing blood pressure. Methyldopa usually produces highly effective lowering of the supine pressure with infrequent symptomatic postural hypotension. Exercise hypotension and diurnal blood pressure variations rarely occur. Methyldopa, in its active metabolite form, is a central alpha-2 receptor agonist. Using methyldopa leads to alpha-2 receptor-negative feedback to sympathetic nervous system (SNS) (centrally and peripherally), allowing peripheral sympathetic nervous system tone to decrease. Such activity leads to a decrease in total peripheral resistance (TPR) and cardiac output. When introduced it was a mainstay of antihypertensive therapy, but its use has declined, with increased use of other safer classes of agents. One of its important present-day uses is in the management of pregnancy-induced hypertension, as it is relatively safe in pregnancy compared to other antihypertensive drugs (Wikipedia).
An alpha-2 adrenergic agonist that has both central and peripheral nervous system effects. Its primary clinical use is as an antihypertensive agent.
Drug Indication
Methyldopa is indicated for the management of hypertension as monotherapy or in combination with hydrochlorothiazide. Methyldopa injection is used to manage hypertensive crises.
FDA Label
Mechanism of Action
The exact mechanism of methyldopa is not fully elucidated; however, the main mechanisms of methyldopa involve its actions on alpha-adrenergic receptor and the aromatic L-amino acid decarboxylase enzyme, to a lesser extent. The sympathetic outflow is regulated by alpha (α)-2 adrenergic receptors and imidazoline receptors expressed on adrenergic neurons within the rostral ventrolateral medulla. Methyldopa is metabolized to α‐methylnorepinephrine via dopamine beta-hydroxylase activity and, consequently, alpha-methylepinephrine via phenylethanolamine-N-methyltransferase activity. Mediating the therapeutic effects of methyldopa, α‐methylnorepinephrine and α-methylepinephrine active metabolites are agonists at presynaptic alpha-2 adrenergic receptors in the brainstem. Stimulating alpha-2 adrenergic receptors results in the inhibition of adrenergic neuronal outflow and attenuation of norepinephrine release in the brainstem. Consequently, the output of vasoconstrictor adrenergic signals to the peripheral sympathetic nervous system is reduced, leading to a reduction in blood pressure. The L-isomer of alpha-methyldopa also reduces blood pressure by inhibiting aromatic L-amino acid decarboxylase, also known as DOPA decarboxylase, which is an enzyme responsible for the syntheses of dopamine and serotonin. Inhibiting this enzyme leads to depletion of biogenic amines such as norepinephrine. However, inhibition of aromatic L-amino acid decarboxylase plays a minimal role in the blood-pressure‐lowering effect of methyldopa.
METHYLDOPA...HAS HYPOTENSIVE ACTION INDEPENDENT OF ITS ANTIADRENERGIC ACTIONS; THIS IS PROBABLY PARTLY CENTRAL DEPRESSANT ACTION @ VASOMOTOR CENTER & PARTLY PERIPHERAL ACTION OF UNKNOWN MECHANISM.
... Alpha-methylnorepinephrine acts in the brain to inhibit adrenergic neuronal outflow from the brainstem, and this central effect is principally responsible for its antihypertensive action.
IN CONSCIOUS RENAL HYPERTENSIVE RATS ALPHA-METHYLDOPA PRODUCED A LONG-LASTING FALL IN BLOOD PRESSURE WHICH WAS PARTIALLY ATTENUATED BY PRETREATMENT WITH NALTREXONE (5 MG/KG SC). PRETREATMENT WITH ANTISERUM TO BETA-ENDORPHIN APPLIED LOCALLY, ALSO BLOCKED THE DEPRESSOR RESPONSE. THESE RESULTS SUGGEST THAT THE FALL IN BLOOD PRESSURE OBSERVED AFTER ALPHA-METHYLDOPA AND ITS ACTIVE METABOLITE ALPHA-METHYLNORADRENALINE INVOLVES A BETA-ENDORPHIN LIKE PEPTIDE; A POSSIBLE SITE OF ACTION IS THE NUCLEUS TRACTUS SOLITARII.
A REVIEW ON THE MECHANISM OF ACTION.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C10H13NO4
Molecular Weight
211.2145
Exact Mass
211.084
Elemental Analysis
C, 56.87; H, 6.20; N, 6.63; O, 30.30
CAS #
555-30-6
Related CAS #
Methyldopa hydrate; 41372-08-1; Methyldopa hydrochloride; 884-39-9
PubChem CID
38853
Appearance
White to off-white solid powder
Density
1.4±0.1 g/cm3
Boiling Point
441.6±45.0 °C at 760 mmHg
Melting Point
≥300 °C
Flash Point
220.9±28.7 °C
Vapour Pressure
0.0±1.1 mmHg at 25°C
Index of Refraction
1.635
LogP
0.13
Hydrogen Bond Donor Count
4
Hydrogen Bond Acceptor Count
5
Rotatable Bond Count
3
Heavy Atom Count
15
Complexity
246
Defined Atom Stereocenter Count
1
SMILES
O([H])C([C@](C([H])([H])[H])(C([H])([H])C1C([H])=C([H])C(=C(C=1[H])O[H])O[H])N([H])[H])=O
InChi Key
CJCSPKMFHVPWAR-JTQLQIEISA-N
InChi Code
InChI=1S/C10H13NO4/c1-10(11,9(14)15)5-6-2-3-7(12)8(13)4-6/h2-4,12-13H,5,11H2,1H3,(H,14,15)/t10-/m0/s1
Chemical Name
(2S)-2-amino-3-(3,4-dihydroxyphenyl)-2-methylpropanoic acid
Synonyms
Dopamet; Dopegit; Dopegyt; Dopergit; Hydopa; Meldopa; Nu-Medopa; Nu Medopa; NuMedopa; Methyldopa; MK-351; MK 351
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO: ~2 mg/mL (~9.5 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In Vivo)
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.

Injection Formulations
(e.g. IP/IV/IM/SC)
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 : PEG300Tween 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 : PEG300Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH 400 μLPEG300 50 μL Tween 80 450 μL Saline)


Oral Formulations
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


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.

 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 4.7346 mL 23.6731 mL 47.3462 mL
5 mM 0.9469 mL 4.7346 mL 9.4692 mL
10 mM 0.4735 mL 2.3673 mL 4.7346 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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Working concentration mg/mL;

Method for preparing DMSO stock solution mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.

Method for preparing in vivo formulation:Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.

(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
             (2) Be sure to add the solvent(s) in order.

Clinical Trial Information
NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT05888896 Recruiting Other: methyldopa tablets 250mg
Other: methyldopa tablets 250mg
+ foot reflexology
Mild Pre-eclampsia Cairo University June 9, 2023 Not Applicable
NCT05211609 Recruiting Diagnostic Test: Plasmatic
3-O-Methyldopa dosage
Aromatic L-Amino Acid
Decarboxylase Deficiency
University Hospital, Montpellier May 20, 2022 Not Applicable
NCT01883804 Completed Drug: Methyldopa Diabetes Mellitus, Type 1 University of Colorado, Denver June 2013 Not Applicable
NCT03210025 Completed Drug: BF-Methyldopa 250mg Tablet
Drug: Metopa Tab 250mg
Healthy Bright Future Pharmaceuticals
Factory O/B Bright Future Pharmaceutical
Laboratories Limited
September 20, 2017 Phase 1
NCT04835233 Completed Drug: Methyldopa 250 MG Hypertension
Postpartum Pre-Eclampsia
Federal University of Paraíba May 1, 2021 Phase 4
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