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Nifedipine (BAY-a-1040)

Alias: BAY-a 1040; BAY a-1040; Adalat, Procardia, Bay-1040, BAY-a-1040;Cordipin, Corinfar, Bay 1040, Bay1040
Cat No.:V1289 Purity: ≥98%
Nifedipine (Adalat, Procardia, Bay-1040,BAY-a-1040;Cordipin, Corinfar, Bay 1040) is a dihydropyridine calcium channel blocker (CCB) with antihypertensive effects.
Nifedipine (BAY-a-1040)
Nifedipine (BAY-a-1040) Chemical Structure CAS No.: 21829-25-4
Product category: GABA Receptor
This product is for research use only, not for human use. We do not sell to patients.
Size Price Stock Qty
2g
5g
10g
25g
Other Sizes
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Purity & Quality Control Documentation

Purity: =99.99%

Product Description

Nifedipine (Adalat, Procardia, Bay-1040, BAY-a-1040; Cordipin, Corinfar, Bay 1040) is a dihydropyridine calcium channel blocker (CCB) with antihypertensive effects. It has been used to lower blood pressure and to treat angina, Raynaud's phenomenon, and premature labor. Nifedipine targets L-type voltage-sensitive calcium channels. Nifedipine is a vasodilator that is selective for inotropic over chronotropic cardiac effects. Nifedipine causes a significant concentration-dependent increase in eNOS protein expression by cultured human coronary artery endothelial cells. Nifedipine antagonizes L-type Ca+ channels found throughout the cardiovascular system, but also blocks Kv channels, which are members of the same supergene family.

Biological Activity I Assay Protocols (From Reference)
ln Vitro
There are no significant differences in viability between the control cells and the cells treated with 100 μM of FAC or 1 and 10 μM of nifedipine. Nifedipine (BAY-a-1040) (1, 10, or 100 μM) significantly increases the iron level in WKPT-0293 Cl.2 cells. Nifedipine (BAY-a-1040) (10 or 100 μM) significantly lowers the viability of the WKPT-0293 Cl.2 Cells. Treatment of nifedipine (10 or 100 μM) plus FAC induces a significant reduction in cell viability. In WKPT-0293 Cl.2 cells, nifedipine treatment also upregulates the expression of TfR1, DMT1+IRE, and DMT1-IRE. Furthermore, co-administration of 100 μM nifedipine and 100 μM FAC results in upregulation of TfR1, DMT1+IRE, and DMT1-IRE expression in WKPT-0293 Cl.2 cells[2]. In the midrange of concentrations, nifedipine plus ritodrine significantly inhibits contractility more than either medication alone. A considerably higher inhibition is produced by nifedipine plus atosiban or nitroglycerin combined than by either drug alone, but not by nifedipine plus atosiban. The inhibitory effect of each drug is lessened when nifedipine and NS-1619 (Ca2+-activated K+ [BKCa] channel opener) are taken together[3]. At 2 μM, nifedipine (BAY-a-1040) dramatically suppresses the growth and sporulation of P. capsici mycelial cells. Calcium is required for the inhibition of mycelial growth caused by nifedipine (BAY-a-1040). P. capsici's sensitivity to H2O2 is increased by nifedipine (0.5 μM) in a calcium-dependent way[4].
ln Vivo
At the conclusion of the fourth week, the BL dimensions (BLi and BLk), MD dimensions (MDk), and vertical dimensions (VHi and VHk) of rats treated with Nifedipine (BAY-a-1040) (50 mg/kg) and CsA show a significant (P < 0.05) increase[1].
Animal Protocol
All the 30 rats are randomLy distributed into three equal groups of ten animals each. Group 1 (control) receive olive oil for the 8 weeks. Group 2 and Group 3 receive a combination of CsA (30 mg/kg body weight) and Nf (50 mg/kg body weight) in olive oil for 8 weeks. In Group 3 rats, Azi (10 mg/kg body weight) is added to this regimen, in the 5th week. The total study period is 8 weeks.
Rats
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
Sublingual dosing leads to a Cmax of 10ng/mL, with a Tmax of 50min, and an AUC of 25ng\*h/mL. Oral dosing leads to a Cmax of 82ng/mL, with a Tmax of 28min, and an AUC of 152ng\*h/mL. Nifedipine is a Biopharmaceutics Classification System Class II drug, meaning it has low solubility and high intestinal permeability. It is almost completely absorbed in the gastrointestinal tract but has a bioavilability of 45-68%, partly due to first pass metabolism.
Nifedipine is 60-80% recovered in the urine as inactive water soluble metabolites, and the rest is eliminated in the feces as metabolites.
The steady state volume of distribution of nifedipine is 0.62-0.77L/kg and the volume of distribution of the central compartment is 0.25-0.29L/kg.
The total body clearance of nifedipine is 450-700mL/min.
Approximately 90% of an oral dose of nifedipine is rapidly absorbed from the GI tract following oral administration of the drug as conventional capsules. Only about 45-75% of an oral dose as conventional capsules reaches systemic circulation as unchanged drug since nifedipine is metabolized on first pass through the liver. Peak serum concentrations usually are reached within 0.5-2 hours after oral administration as conventional capsules. Food appears to decrease the rate but not the extent of absorption of nifedipine as conventional capsules.
Plasma drug concentrations rise at a gradual, controlled rate after a nifedipine extended-release tablet dose and reach a plateau at approximately six hours after the first dose. For subsequent doses, relatively constant plasma concentrations at this plateau are maintained with minimal fluctuations over the 24-hour dosing interval. About a four-fold higher fluctuation index (ratio of peak to trough plasma concentration) was observed with the conventional immediate-release nifedipine capsule at t.i.d. dosing than with once daily nifedipine extended-release tablet.
At steady-state the bioavailability of the nifedipine extended-release tablet is 86% relative to immediate-release nifedipine capsules. Administration of the nifedipine extended-release tablet in the presence of food slightly alters the early rate of drug absorption, but does not influence the extent of drug bioavailability. Markedly reduced GI retention time over prolonged periods (ie, short bowel syndrome), however, may influence the pharmacokinetic profile of the drug which could potentially result in lower plasma concentrations.
The manufacturer states that relative oral bioavailability differs little if conventional nifedipine capsules are swallowed intact, bitten and swallowed, or bitten and held sublingually. However, some data indicate that the rate and extent of absorption of nifedipine following sublingual administration may be decreased substantially. Oral bioavailability of nifedipine may be increased up to twofold in patients with liver cirrhosis.
For more Absorption, Distribution and Excretion (Complete) data for Nifedipine (10 total), please visit the HSDB record page.
Metabolism / Metabolites
Nifedipine is predominantly metabolized by CYP3A4. Nifedipine is predominantly metabolized to 2,6-dimethyl-4-(2-nitrophenyl)-5-methoxycarbonyl-pyridine-3-carboxylic acid, and then further metabolized to 2-hydroxymethyl-pyridine carboxylic acid. Nifedipine is also minorly metabolized to dehydronifedipine.
The drug is extensively metabolized in the liver (to highly water-soluble, inactive metabolites) by the cytochrome P-450 microsomal enzyme system, including CYP3A.
Nifedipine has known human metabolites that include Oxidized nifedipine.
Biological Half-Life
The terminal elimination half life of nifedipine is approximately 2 hours.
In patients with normal renal and hepatic function, the plasma half-life of nifedipine is about 2 hours when administered as conventional capsules, and about 7 hours when administered as extended-release tablets (Adalat CC).
Toxicity/Toxicokinetics
Interactions
Quinidine is a substrate of CYP3A and has been shown to inhibit CYP3A in vitro. Co-administration of multiple doses of quinidine sulfate, 200 mg t.i.d., and nifedipine, 20 mg t.i.d., increased Cmax and AUC of nifedipine in healthy volunteers by factors of 2.30 and 1.37, respectively. The heart rate in the initial interval after drug administration was increased by up to 17.9 beats/minute. The exposure to quinidine was not importantly changed in the presence of nifedipine. Monitoring of heart rate and adjustment of the nifedipine dose, if necessary, are recommended when quinidine is added to a treatment with nifedipine.
Pre-treatment of healthy volunteers with 30 mg or 90 mg t.i.d. diltiazem p.o. increased the AUC of nifedipine after a single dose of 20 mg nifedipine by factors of 2.2 and 3.1, respectively. The corresponding Cmax values of nifedipine increased by factors of 2.0 and 1.7, respectively. Caution should be exercised when co-administering diltiazem and nifedipine and a reduction of the dose of nifedipine should be considered.
Verapamil, a CYP3A inhibitor, can inhibit the metabolism of nifedipine and increase the exposure to nifedipine during concomitant therapy. Blood pressure should be monitored and reduction of the dose of nifedipine considered.
In healthy volunteers receiving single dose of 20 mg nifedipine ER and benazepril 10 mg, the plasma concentrations of benazeprilat and nifedipine in the presence and absence of each other were not statistically significantly different. A hypotensive effect was only seen after co-administration of the two drugs. The tachycardic effect of nifedipine was attenuated in the presence of benazepril.
For more Interactions (Complete) data for Nifedipine (22 total), please visit the HSDB record page.
Non-Human Toxicity Values
LD50 Rat oral 1022 mg/kg
LD50 Rat ip 230 mg/kg
LD50 Mouse oral 310 mg/kg
LD50 Mouse ip 185 mg/kg
LD50 Rabbit oral 504 mg/kg
References
[1]. Ratre MS, et al. Effect of azithromycin on gingival overgrowth induced by cyclosporine A + nifedipine combination therapy: A morphometric analysis in rats. J Indian Soc Periodontol. 2016 Jul-Aug;20(4):396-401.
[2]. Carvajal JA, et al. The Synergic In Vitro Tocolytic Effect of Nifedipine Plus Ritodrine on Human Myometrial Contractility. Reprod Sci. 2017 Apr;24(4):635-640.
[3]. Yu SS, et al. Nifedipine Increases Iron Content in WKPT-0293 Cl.2 Cells via Up-Regulating Iron Influx Proteins. Front Pharmacol. 2017 Feb 13;8:60
[4]. Liu P, et al. The L-type Ca(2+) Channel Blocker Nifedipine Inhibits Mycelial Growth, Sporulation, and Virulence of Phytophthora capsici. Front Microbiol. 2016 Aug 4;7:1236
Additional Infomation
Therapeutic Uses
Calcium Channel Blockers; Tocolytic Agents; Vasodilator Agents
Nifedipine extended-release tablets are indicated for the management of vasospastic angina confirmed by any of the following criteria: 1) classical pattern of angina at rest accompanied by ST segment elevation, 2) angina or coronary artery spasm provoked by ergonovine, or 3) angiographically demonstrated coronary artery spasm. In those patients who have had angiography, the presence of significant fixed obstructive disease is not incompatible with the diagnosis of vasospastic angina, provided that the above criteria are satisfied. Nifedipine extended-release may also be used where the clinical presentation suggests a possible vasospastic component but where vasospasm has not been confirmed, eg, where pain has a variable threshold on exertion or in unstable angina where electrocardiographic findings are compatible with intermittent vasospasm, or when angina is refractory to nitrates and/or adequate doses of beta blockers. /Included in US product label/
Nifedipine extended-release tablets are indicated for the management of chronic stable angina (effort-associated angina) without evidence of vasospasm in patients who remain symptomatic despite adequate doses of beta blockers and/or organic nitrates or who cannot tolerate those agents. /Included in US product label/
Nifedipine extended-release tablets (ADALAT CC) is indicated for the treatment of hypertension. It may be used alone or in combination with other antihypertensive agents. /Included in US product label/
Drug Warnings
The National Heart, Lung, and Blood Institute (NHLBI) concluded from the apparent concordance of findings from observational studies in hypertensive patients and from randomized studies principally in acute myocardial infarction and unstable angina patients that it seems prudent and consistent with current evidence to recommend that short-acting nifedipine, especially at high doses, be used in the management of hypertension, angina, or myocardial infarction with great caution, if at all.
The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), which compared long-term therapy with an ACE inhibitor (lisinopril) or dihydropyridine-derivative calcium-channel blocker (amlodipine) revealed no difference in the primary outcome of combined fatal coronary heart disease or nonfatal myocardial infarction among these therapies.
Serious adverse reactions requiring discontinuance of nifedipine therapy or dosage adjustment are relatively rare. An increase in the frequency, intensity, and duration of angina, possibly resulting from hypotension, has occurred rarely during initiation of nifedipine therapy. Additional serious adverse effects including myocardial infarction, congestive heart failure or pulmonary edema, and ventricular arrhythmia or conduction defects have reportedly occurred in 4%, 2%, and less than 0.5% of patients receiving conventional nifedipine capsules, respectively, but these have not been directly attributed to the drug.
Rarely, patients, usually receiving a beta blocker, have developed heart failure after beginning nifedipine. Patients with tight aortic stenosis may be at greater risk for such an event, as the unloading effect of nifedipine would be expected to be of less benefit to those patients, owing to their fixed impedance to flow across the aortic valve.
For more Drug Warnings (Complete) data for Nifedipine (32 total), please visit the HSDB record page.
Pharmacodynamics
Nifedipine is an inhibitor of L-type voltage gated calcium channels that reduces blood pressure and increases oxygen supply to the heart. Immediate release nifedipine's duration of action requires dosing 3 times daily. Nifedipine dosing is generally 10-120mg daily. Patients should be counselled regarding the risk of excessive hypotension, angina, and myocardial infarction.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C17H18N2O6
Molecular Weight
346.33
Exact Mass
346.116
CAS #
21829-25-4
Related CAS #
21829-25-4(Nifedipine);
PubChem CID
4485
Appearance
Yellow crystals
Density
1.3±0.1 g/cm3
Boiling Point
475.3±45.0 °C at 760 mmHg
Melting Point
171-175 °C
Flash Point
241.2±28.7 °C
Vapour Pressure
0.0±1.2 mmHg at 25°C
Index of Refraction
1.559
LogP
2.97
Hydrogen Bond Donor Count
1
Hydrogen Bond Acceptor Count
7
Rotatable Bond Count
5
Heavy Atom Count
25
Complexity
608
Defined Atom Stereocenter Count
0
SMILES
O(C([H])([H])[H])C(C1=C(C([H])([H])[H])N([H])C(C([H])([H])[H])=C(C(=O)OC([H])([H])[H])C1([H])C1=C([H])C([H])=C([H])C([H])=C1[N+](=O)[O-])=O
InChi Key
HYIMSNHJOBLJNT-UHFFFAOYSA-N
InChi Code
InChI=1S/C17H18N2O6/c1-9-13(16(20)24-3)15(14(10(2)18-9)17(21)25-4)11-7-5-6-8-12(11)19(22)23/h5-8,15,18H,1-4H3
Chemical Name
dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate
Synonyms
BAY-a 1040; BAY a-1040; Adalat, Procardia, Bay-1040, BAY-a-1040;Cordipin, Corinfar, Bay 1040, Bay1040
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

Note: This product requires protection from light (avoid light exposure) during transportation and storage.
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:69 mg/mL (199.2 mM)
Water:<1 mg/mL
Ethanol:15 mg/mL (43.3 mM)
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 2.5 mg/mL (7.22 mM) (saturation unknown) in 10% DMSO + 40% PEG300 +5% Tween-80 + 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 25.0 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.

 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 2.8874 mL 14.4371 mL 28.8742 mL
5 mM 0.5775 mL 2.8874 mL 5.7748 mL
10 mM 0.2887 mL 1.4437 mL 2.8874 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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Clinical Trial Information
Treatment of Elevated Blood Pressures in Early Pregnancy
CTID: NCT05955040
Phase: Phase 2    Status: Terminated
Date: 2024-11-21
Pharmacokinetics and Safety of Commonly Used Drugs in Lactating Women and Breastfed Infants
CTID: NCT03511118
Phase:    Status: Recruiting
Date: 2024-07-24
Treating Postictal Symptoms Using Ibuprofen and Nifedipine
CTID: NCT03949478
Phase: Phase 2    Status: Recruiting
Date: 2024-05-09
Safest Choice of Antihypertensive Regimen for Postpartum Hypertension
CTID: NCT05551104
Phase: Phase 3    Status: Recruiting
Date: 2024-05-06
Postpartum Hypertension Study
CTID: NCT05139238
Phase: Phase 4    Status: Not yet recruiting
Date: 2024-03-18
View More

Effect of Labetalol, Atenolol, and Nifedipine on Maternal Hemodynamics Measured by ICG in Early Pregnancy
CTID: NCT04755764
Phase:    Status: Recruiting
Date: 2024-03-13


Comparative Study of Intravenous Labetalol Versus Intravenous Nitroglycerin Versus Sublingual Nifedipine
CTID: NCT06265415
Phase: N/A    Status: Not yet recruiting
Date: 2024-02-20
Tocolysis in the Management of Preterm Premature Rupture of Membranes Before 34 Weeks of Gestation
CTID: NCT03976063
Phase: Phase 3    Status: Recruiting
Date: 2024-02-13
Evaluating the Utility of Continuous Positive Airway Pressure in the Treatment of High Altitude Pulmonary Edema
CTID: NCT04186598
Phase: N/A    Status: Completed
Date: 2024-02-07
Nifedipine Plus Magnesium Sulfate Versus Magnesium Sulfate for Very Early Preterm Tocolysifs
CTID: NCT05345132
Phase: N/A    Status: Recruiting
Date: 2023-12-08
Nifedipine Versus Magnesium Sulfate for Late Preterm Tocolysis
CTID: NCT05343806
Phase: N/A    Status: Recruiting
Date: 2023-12-08
Nifedipine XL Versus Placebo for the Treatment of Preeclampsia With Severe Features During Induction of Labor
CTID: NCT04392375
Phase: Phase 4    Status: Completed
Date: 2023-07-24
Effects Of Sitaxsentan On Proteinuria, 24-Hour Blood Pressure, And Arterial Stiffness In Chronic Kidney Disease Subjects
CTID: NCT00810732
Phase: Phase 2    Status: Completed
Date: 2023-07-06
Medicine-induced Cardiac Hemodialysis on COVID-19
CTID: NCT05711810
Phase: Phase 4    Status: Completed
Date: 2023-02-03
The Treatment of Magnesium Sulfate and Nifedipine in Preterm Labor Threat
CTID: NCT05520021
Phase: N/A    Status: Unknown status
Date: 2022-09-15
Is Procardia XL 60 mg Q Daily Equivalent to 30 mg XL Given Twice Daily?
CTID: NCT03595982
Phase: Phase 4    Status: Terminated
Date: 2022-06-30
Nifedipine or Nifedipine Plus Indomethacin for Treatment of Acute Preterm Labor
CTID: NCT02438371
Phase: Phase 4    Status: Terminated
Date: 2021-11-24
Comparison of Nifedipine Versus Indomethacin for Acute Preterm Labor
CTID: NCT03129945
Phase: N/A    Status: Completed
Date: 2021-11-05
Nifedipine Versus Magnesium Sulfate for Prevention of Preterm Labor in Symptomatic Placenta Previa
CTID: NCT03542552
Phase: Phase 3    Status: Completed
Date: 2021-07-28
Role of Calcium Channels in Vascular Function
CTID: NCT02885558
Phase: N/A    Status: Completed
Date: 2021-06-01
Response to Anti-hypertensives in Pregnant and Postpartum Patients
CTID: NCT03506724
Phase: Phase 4    Status: Completed
Date: 2021-05-24
Early Vascular Adjustments During Hypertensive Pregnancy
CTID: NCT02531490
Phase: Phase 4    Status: Unknown status
Date: 2021-03-24
Nifedipine for Acute Tocolysis of Preterm Labor
CTID: NCT02132533
Phase: Phase 3    Status: Completed
Date: 2020-12-21
The Efficacy of Nifedipine in the Management of Preterm Labor
CTID: NCT04644354
Phase:    Status: Unknown status
Date: 2020-11-25
Non-Invasive Positive Pressure Ventilation Management of High Altitude Pulmonary Edema
CTID: NCT04288219
Phase: N/A    Status: Unknown status
Date: 2020-09-03
Vaginal Indomethacin for Preterm Labor
CTID: NCT04404686
PhaseP
Pregnancy And chronic hypertension: NifeDipine or labetalol as Antihypertensive treatment
CTID: null
Phase: Phase 4    Status: Completed
Date: 2014-02-03
A Multicenter, Randomized, Double-Blind, Monotherapy-Controlled Study of Nifedipine Gastrointestinal Therapeutic System and Candesartan Cilexetil in Combination Taken Orally for 8 Weeks in Adult Subjects with Essential Hypertension who are Inadequately Controlled on Nifedipine Gastrointestinal Therapeutic System Monotherapy
CTID: null
Phase: Phase 3    Status: Prematurely Ended, Completed
Date: 2013-09-19
A Multicenter, Randomized, Double-Blind, Monotherapy-Controlled Study of Nifedipine Gastrointestinal Therapeutic System and Candesartan Cilexetil in Combination Taken Orally for 8 Weeks in Adult Subjects with Essential Hypertension Who Are Inadequately Controlled on 16 mg Candesartan Cilexetil Monotherapy
CTID: null
Phase: Phase 3    Status: Prematurely Ended, Completed
Date: 2013-07-31
Lymphatic dysfunction as a cause of calcium channel blocker oedema
CTID: null
Phase: Phase 3    Status: Completed
Date: 2013-05-21
Nifedipine versus Atosiban in the treatment of threatened preterm labour
CTID: null
Phase: Phase 4    Status: Ongoing
Date: 2012-11-23
UTILITY OF THE ocolytict MAINTENANCE TREATMENT IN THE MANAGEMENT OF THE THREAT OF PREMATURE
CTID: null
Phase: Phase 3    Status: Prematurely Ended
Date: 2012-11-13
Assessment of Perinatal Outcome by uSe of Tocolysis in Early Labour (APOSTEL IV); Nifedipine versus placebo in the treatment of preterm premature rupture of membranes
CTID: null
Phase: Phase 3    Status: Prematurely Ended
Date: 2012-02-07
A Multicenter, Multifactorial, Randomized, Double-Blind, Placebo-Controlled Dose-
CTID: null
Phase: Phase 2    Status: Completed
Date: 2011-03-28
Use of drug therapy in the management of symptomatic ureteric stones in hospitalised adults: a multicentre placebo controlled randomised trial of a calcium channel blocker(nifedipine)and an alpha blocker(tamsulosin) - The SUSPEND trial
CTID: null
Phase: Phase 4    Status: Completed
Date: 2010-07-29
EFFECTS OF NIFEDIPINE ON IRON HOMEOSTASIS IN PATIENTS SUFFERING FROM IRONOVERLOAD DISEASES -
CTID: null
Phase: Phase 3    Status: Prematurely Ended
Date: 2009-08-06
Efficacy and tolerability of a 0.25%glyceryl trinitrate ointment in the treatment of chronic rectal fissures.A multicentric, randomised, open study,controlled vs. Antrolin cream.
CTID: null
Phase: Phase 3    Status: Prematurely Ended
Date: 2008-03-27
A multicenter Study Evaluating the Efficacy of Nifedipine GITS ヨ Telmisartan Combination in Blood Pressure Control and Beyond: comparison of two strategies.
CTID: null
Phase: Phase 4    Status: Completed
Date: 2007-08-29
Maternal and fetal haemodynamic response to Nifedipine tocolysis in normotensive pregnant women.
CTID: null
Phase: Phase 4    Status: Ongoing
Date: 2007-08-23
The effects of sitaxsentan once daily dosing on proteinuria, 24 hour systemic blood pressure and arterial stiffness in subjects with chronic kidney disease.
CTID: null
Phase: Phase 2    Status: Completed
Date: 2007-08-15
To study the cardiovasculair effects of vasodilatation by nifedipine (Adalat gastrointestinal therapeutic system) with or without plasma volume expansion with Voluven (colloid) in women with preeclampsia
CTID: null
Phase: Phase 4    Status: Prematurely Ended
Date: 2007-02-12
Preliminary evaluation of efficacy and tolerability of the association mesalazine 1g nifedipine 10mg in the treatment of tenesmus in patients suffering of distal ulcerative cholitis. Open study, phase II, two steps according to Simon
CTID: null
Phase: Phase 2    Status: Completed
Date: 2006-12-21
Multicenter, Open-Label, Long-Term Safety and Efficacy Study of the Fixed Dose Combination of Nifedipine Gastrointestinal Therapeutic System and Candesartan Cilexetil in Adult Subjects with Moderate to Severe Essential Hypertension
CTID: null
Phase: Phase 3    Status: Completed
Date:
Clinical study on the resistance to antihypertensive therapy in patients with diabetes mellitus
CTID: UMIN000003195
Phase:    Status: Complete: follow-up complete
Date: 2010-02-17
Microdosing cinical studies -Assesment of oral bioavailability of drugs by cassete IV and PO dosing-
CTID: UMIN000002578
PhaseNot applicable    Status: Recruiting
Date: 2009-10-03
An open label multi facilities cooperation randomized control trial to verify urinary angiotensinogen excretion reducing effect of olmesartan therapy in diabetic nephropathy.
CTID: UMIN000001618
Phase:    Status: Complete: follow-up complete
Date: 2009-03-09
The influence of azelnidipine on plasma renin activity and plasma aldosterone concentration in hypertensive patients.
CTID: UMIN000001739
Phase:    Status: Complete: follow-up complete
Date: 2009-02-27
Comparison of therapeutic effects of long-acting calcium channel blockers on coronary vasospasm.; Open label randomized trial (ATTACK VSA TRIAL)
CTID: UMIN000001105
PhaseNot applicable    Status: Complete: follow-up complete
Date: 2008-04-01
Short Treatment with the Angiotensin Receptor Blocker Candesartan Surveyed by Telemedicine
CTID: UMIN000000941
Phase:    Status: Complete: follow-up complete
Date: 2008-04-01

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