PainPhase 1NCT01676246
Pharmacokinetics, Metabolism and Analgesic Effects of Flupirtine
A Phase 1 study testing 100 mg flupirtine intravenous, 100 mg flupirtine per os and 400 mg flupirtine per os in people with Pain and Pharmacokinetics, run by University Medicine Greifswald at 1 site in Germany.
Trial summary
Flupirtine is metabolized in-vitro via carbamate cleavage and N acetylation to glucuronides and mercapturic acid derivatives. The formation of reactive, toxic intermediate products may be influenced by genetic polymorphisms of the involved conjugative metabolic pathways. Read more about this study
- Who is it for?
- Ages 18 to 45 yearsHealthy volunteers can take part
- Conditions the study is for
- Pain, Pharmacokinetics, Flupirtine
- What is being tested?
- 100 mg flupirtine intravenous, 100 mg flupirtine per os and 400 mg flupirtine per os
- Type of treatment
- Pill or oral medicine, Injection or infusion, Surgery or procedure
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 36 participants
- Where
- 1 siteGermany
- Study dates
- May 2008to Jun 2009
- Phase
- Phase 1
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 45 years
- All sexes
- Healthy volunteers accepted
- Adult
Who may be able to join
- age: 18 - 45 years
- sex and genetics: male and female genotyped for NAT2, UGT1A1 and GSTP1
- ethnic origin: Whites
- body weight: 19 - 27 kg/m²
- good health as evidenced by the results of the clinical examination, ECG, and the laboratory check-up, which are judged by the clinical investigator not to differ in a clinical relevant way from the normal state
- written informed consent
Who cannot join
- existing cardiac or hematological diseases and/or pathological findings which might interfere with safety, pharmacodynamic effect and/or pharmacokinetics of the study drug
- existing or further obstructive lung disease (e.g. bronchial asthma)
- myasthenia gravis
- existing hepatic and renal diseases and/or pathological findings which might interfere with safety, pharmacodynamic effect and/or pharmacokinetics of the study drug
- existing gastrointestinal diseases and/or pathological findings which might interfere with safety, pharmacodynamic effect and/or pharmacokinetics of the study drug
- acute or chronic diseases which could affect drug absorption or metabolism
Show all 26Show fewer
- history of any serious psychological disorder
- drug or alcohol dependence
- positive drug screening or -only in suspicious case- positive alcohol test
- smokers of 10 or more cigarettes per day
- positive screening results for HIV, HBV and HCV
- volunteers who are on a diet which could affect the pharmacokinetics of the drug (vegetarian)
- heavy tea or coffee drinkers (more than 1l per day)
- lactation and pregnancy test positive or not performed
- volunteers suspected or known not to follow instructions
- volunteers who are unable to understand the written and verbal instructions, in particular regarding the risks and inconveniences they will be exposed to as a result of their participation in the study
- volunteers liable to orthostatic dysregulation, fainting, or blackouts
- blood donation or other blood loss of more than 400 ml within the last 12 weeks prior to the start of the study
- participation in a clinical trial during the last 3 months prior to the start of the study
- less than 14 days after last acute disease
- any systemically available medication within 4 weeks prior to the intended first administration unless, because of the terminal elimination half-life, complete elimination from the body can be assumed for the drug and/or its primary metabolites (except oral contraceptives)
- repeated use of drugs during the last 4 weeks prior to the intended first administration, which can influence hepatic biotransformation (e.g. barbiturates, cimetidine, phenytoin, rifampicin)
- repeated use of drugs during the last 2 weeks prior to the intended first administration which affect absorption (e.g. laxatives, metoclopramide, loperamide, antacids, H2-receptor antagonists)
- intake of grapefruit containing food or beverages within 7 days prior to administration
- known allergic reactions to the active ingredients used or to constituents of the pharmaceutical preparation
- subjects with severe allergies or multiple drug allergies
Trial locations and contacts
1 site in 1 country.
Germany1 site
Department of Clinical Pharmacology, Ernst-Moritz-Arndt-University Greifswald
Greifswald, Mecklenburg-Vorpommern, 17487
About this study
Official title: Pharmacokinetics, Metabolism and Analgesic Effects of Flupirtine After Intravenous, Single Dose and Chronic Oral Administration in Healthy Subjects Genotyped for NAT2, UGT1A1 and GSTP1
Flupirtine is metabolized in-vitro via carbamate cleavage and N acetylation to glucuronides and mercapturic acid derivatives. The formation of reactive, toxic intermediate products may be influenced by genetic polymorphisms of the involved conjugative metabolic pathways. So the purpose of this study is to measure pharmacokinetics, metabolism and analgesic effects of flupirtine in dependence on the function of NAT2, UGT1A1 and GSTP1.
Read the detailed description
Flupirtine is a centrally acting analgesic drug. Its mechanism of action differs obviously from opiates because flupirtine antagonizes the morphine-induced tail phenomenon in mice in relatively low doses. The drug exerts no relevant anesthetic activity and it has only slight inhibitory effect on prostaglandin formation in animals. As major action mechanism, activation of descending noradrenergic neuronal pathways is discussed, thereby inhibiting afferent nociceptive stimuli on spinal, subcortical and cortical brain areas. Recently has been shown, that flupirtine exhibits functional NMDA receptor antagonistic properties by selective opening the neuronal potassium channel.
The anticonvulsant drug retigabine, which chemical structure only slightly differs from flupirtine (aromatic ring instead of the pyrimidine ring), is subjected to intensive glucuronidation and N-acetylation in man. In-vitro, retigabine is a substrate of the recombinant uridine glucoronosyl transferase (UGT) 1A1, 1A3, 1A4 and 1A9. Disposition of retigabine, however, was not influenced by the frequent UGT1A1*28 polymorphism (Gilbert-Meulengracht syndrome) whereas the polymorphism of the N-acetyltransferase 2 (NAT2) resulted in significant changes in retigabine disposition.
Similar to retigabine, the carbamate group of flupirtine is hydrolyzed by carboxyl esterases. The decarbamylated product undergoes N-acetylation to form the major metabolite D13223. This acetylation is catalyzed in-vitro both by recombinant human NAT2 and NAT1. Furthermore, relatively stable quinone diimines for flupirtine and D13223 as catalyzed by peroxidases were detectable in in-vitro experiments. After repeated oral administration of flupirtine in man, quinone diimines and glutathione adducts of them in the form of mercapturic acid conjugates were detected.
Therefore, we hypothesize, that highly reactive diimine radicals may appear as intermediates which are detoxified by conjugation with glutathione via a glutathione S-transferase (GST). Diimine intermediates are known to have high cell toxicity, genotoxicity and carcinogenicity as shown for the intermediates of acetaminophen. By analogy to acetaminophen, the GSTP1 might be the isoform that is involved also in detoxification of flupirtine intermediates.
According to our hypothesis, the net appearance of toxic intermediates with diimine structure in hepatocytes is dependent on the activity of NAT1/NAT2, UGTs and GSTP1. Because NAT2, UGT1A1 and GSTP1 are highly polymorphic enzymes, the risk of flupirtine hepatotoxicity may be dependent on the genotype of the subjects that are treated with the drug.
Our clinical study was initiated to confirm, whether polymorphisms of NAT2, UGT1A1 and GSTP1 may significantly influence disposition and analgesic effect of flupirtine and whether the genetic background is of risk for the appearance of toxic intermediates and its stable terminal conjugates.
- Conditions
- Pain, Pharmacokinetics, Flupirtine
- Being tested
- 100 mg flupirtine intravenous, 100 mg flupirtine per os, 400 mg flupirtine per os, induce delayed onset of muscle soreness (DOMS), electric pain measurement
- Medical subject headings
- Pain
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
100 mg flupirtine intravenousDrug
Also called 1 vial Kadadolon® inject
Administration of 100 mg flupirtine intravenous (3 mg solution intravenously, 1 vial Kadadolon® inject)
100 mg flupirtine per osDrug
Also called 1 capsule Kadadolon®
Administration of 100 mg flupirtine per os (1 capsule Kadadolon®)
400 mg flupirtine per osDrug
Also called 1 Kadadolon® S long retard tablet
Administration of 400 mg flupirtine (1 Kadadolon® S long retard tablet)
induce delayed onset of muscle soreness (DOMS)Procedure or surgery
The DOMS exercise protocol consists of two sets of 50 concentric/eccentric contractions of the calf muscles of one leg with a rest of 5 min in-between. The exercise is performed 22-26 h prior to medication. For pain measurements, muscle pain is stimulated by standing on tiptoes of one leg for 30 s, which requires a constriction of the affected calf muscles. The other leg is lifted and the subjects are allowed to hold on to a table to keep their balance. The pain intensity during this stimulation is then rated by means of a 10 cm visual analogue scale (VAS). The VAS is extended from "no pain" to "intolerable pain" with a precision of 1 mm. The stimulation is repeated with the other leg. The sequence of the legs is chosen randomly.
electric pain measurementProcedure or surgery
The method has been described to be sensitive to quantify analgesic opioid effects. Painful 5 Hz sine waves electrical stimuli (increase of intensity 0.2 mA/s, from 0 to 20 mA), which predominantly activate C-fibres, will be applied via two gold electrodes placed on the medial and lateral side of the distal phalangeal joint (middle finger of the left hand as default-testing site).
During testing, subjects keep a button continuously pressed until they find the pain intolerably and interrupt the current by releasing the button. The electrical current at which this occurred is defined as pain tolerance, the target parameter of this pain model. Each value of pain tolerance is the median of five subsequent measurements obtained at an interval of 1 min.
| Study group | Role | What they receive |
|---|---|---|
| flupirtine per os single dose | Active comparator | 100 mg flupirtine per os, pharmacokinetics of flupirtine, induce delayed onset of muscle soreness (DOMS), electric pain measurement Receives: Drug: 100 mg flupirtine per os; Procedure: induce delayed onset of muscle soreness (DOMS); Procedure: electric pain measurement |
| flupirtine intravenous | Active comparator | 100 mg flupirtine intravenous, pharmacokinetics of flupirtine, induce delayed onset of muscle soreness (DOMS), electric pain measurement Receives: Drug: 100 mg flupirtine intravenous; Procedure: induce delayed onset of muscle soreness (DOMS); Procedure: electric pain measurement |
| flupirtine per os steady state | Active comparator | 400 mg flupirtine per os, pharmacokinetics of flupirtine, electric pain measurement Receives: Drug: 400 mg flupirtine per os; Procedure: electric pain measurement |
What is being measured
The primary outcome is the main question the study is designed to answer.
bioavailability (F)
ratio of the area under the concentration time curve after oral to intravenous administration of study medication
Measured: before and 0.5,1,1.5,2,2.5,3,3.5,4,5,6,8,10,12,16,24,48,72,96,120 h after administration of study medication
delayed onset of muscle soreness (DOMS)
For pain measurements, muscle pain is stimulated by standing on tiptoes of one leg for 30 s, which requires a constriction of the affected calf muscles. The other leg is lifted and the subjects are allowed to hold on to a table to keep their balance. The pain intensity during this stimulation is then rated by means of a 10 cm visual analogue scale (VAS). The VAS is extended from "no pain" to "intolerable pain" with a precision of 1 mm.
Measured: before and 2, 4, 6, 8 h after study medication
electric pain threshold
A painful 5 Hz sine waves electrical stimuli (increase of intensity 0.2 mA/s, from 0 to 20 mA), will be applied via two gold electrodes placed on the medial and lateral side of the distal phalangeal joint (middle finger of the left hand as default-testing site). During testing, subjects keep a button continuously pressed until they find the pain intolerably and interrupt the current by releasing the button. The electrical current at which this occurred is defined as pain tolerance, the target parameter of this pain model. Each value of pain tolerance is the median of five subsequent measurements obtained at an interval of 1 min.
Measured: before and 2, 4, 6, 8 h (and 10, 12 h on study day 8) after study medication and on study days 1,2,3,4,5,6,7
Secondary outcomes (2)
amount of excretion (Ae) in urine
urinary excretion of flupirtine, D13223 and metabolites
Measured: in 24 h intervals for 3 days
amount of excretion (Ae) of feces
fecal excretion of flupirtine, D13223 and metabolites
Measured: 5 day sampling period
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted30 Aug 2012 (estimated)
- Study startMay 2008
- Primary completionMay 2009
- Study completionJun 2009
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Other trials for PainStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase 1
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- None (open label)
- Enrolment
- 36 participants (actual)
Sponsor and investigators
- Lead sponsor
- University Medicine Greifswald
- Sponsor type
- University, hospital or other
- Collaborators
- AWD.pharma GmbH & Co. KG
- Responsible party
- Principal investigator, Prof. Werner Siegmund, University Medicine Greifswald
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT01676246
- Sponsor's protocol ID
- Flpmetab2008
- Status last verified
- Aug 2012
- First submitted
- 28 Aug 2012
- Last updated
- 30 Aug 2012
- Results posted
- No
- Data monitoring committee
- No
Study at a glance
From the registry record, last updated by the sponsor on 30 Aug 2012. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Pharmacokinetics, Metabolism and Analgesic Effects of Flupirtine After Intravenous, Single Dose and Chronic Oral Administration in Healthy Subjects Genotyped for NAT2, UGT1A1 and GSTP1
- ClinicalTrials.gov ID
- NCT01676246
- Acronym / sponsor ID
- Flpmetab2008
- Conditions
- Pain, Pharmacokinetics, Flupirtine
- Phase
- Phase 1
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 36 participants (actual)
- Lead sponsor
- University Medicine GreifswaldUniversity, hospital or other
- Collaborators
- AWD.pharma GmbH & Co. KG
- Study start
- May 2008
- Primary completion
- May 2009 (actual)
- Study completion
- Jun 2009 (actual)
- First posted
- 30 Aug 2012 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Flupirtine is metabolized in-vitro via carbamate cleavage and N acetylation to glucuronides and mercapturic acid derivatives. The formation of reactive, toxic intermediate products may be influenced by genetic polymorphisms of the involved conjugative metabolic pathways. So the purpose of this study is to measure pharmacokinetics, metabolism and analgesic effects of flupirtine in dependence on the function of NAT2, UGT1A1 and GSTP1.
Detailed description
Flupirtine is a centrally acting analgesic drug. Its mechanism of action differs obviously from opiates because flupirtine antagonizes the morphine-induced tail phenomenon in mice in relatively low doses. The drug exerts no relevant anesthetic activity and it has only slight inhibitory effect on prostaglandin formation in animals. As major action mechanism, activation of descending noradrenergic neuronal pathways is discussed, thereby inhibiting afferent nociceptive stimuli on spinal, subcortical and cortical brain areas. Recently has been shown, that flupirtine exhibits functional NMDA receptor antagonistic properties by selective opening the neuronal potassium channel.
The anticonvulsant drug retigabine, which chemical structure only slightly differs from flupirtine (aromatic ring instead of the pyrimidine ring), is subjected to intensive glucuronidation and N-acetylation in man. In-vitro, retigabine is a substrate of the recombinant uridine glucoronosyl transferase (UGT) 1A1, 1A3, 1A4 and 1A9. Disposition of retigabine, however, was not influenced by the frequent UGT1A1*28 polymorphism (Gilbert-Meulengracht syndrome) whereas the polymorphism of the N-acetyltransferase 2 (NAT2) resulted in significant changes in retigabine disposition.
Similar to retigabine, the carbamate group of flupirtine is hydrolyzed by carboxyl esterases. The decarbamylated product undergoes N-acetylation to form the major metabolite D13223. This acetylation is catalyzed in-vitro both by recombinant human NAT2 and NAT1. Furthermore, relatively stable quinone diimines for flupirtine and D13223 as catalyzed by peroxidases were detectable in in-vitro experiments. After repeated oral administration of flupirtine in man, quinone diimines and glutathione adducts of them in the form of mercapturic acid conjugates were detected.
Therefore, we hypothesize, that highly reactive diimine radicals may appear as intermediates which are detoxified by conjugation with glutathione via a glutathione S-transferase (GST). Diimine intermediates are known to have high cell toxicity, genotoxicity and carcinogenicity as shown for the intermediates of acetaminophen. By analogy to acetaminophen, the GSTP1 might be the isoform that is involved also in detoxification of flupirtine intermediates.
According to our hypothesis, the net appearance of toxic intermediates with diimine structure in hepatocytes is dependent on the activity of NAT1/NAT2, UGTs and GSTP1. Because NAT2, UGT1A1 and GSTP1 are highly polymorphic enzymes, the risk of flupirtine hepatotoxicity may be dependent on the genotype of the subjects that are treated with the drug.
Our clinical study was initiated to confirm, whether polymorphisms of NAT2, UGT1A1 and GSTP1 may significantly influence disposition and analgesic effect of flupirtine and whether the genetic background is of risk for the appearance of toxic intermediates and its stable terminal conjugates.
Study design
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- None (open label)
- Number of arms
- 3
| Arm | Type | Receives |
|---|---|---|
| flupirtine per os single dose | Active comparator | Drug: 100 mg flupirtine per os, Procedure: induce delayed onset of muscle soreness (DOMS), Procedure: electric pain measurement100 mg flupirtine per os, pharmacokinetics of flupirtine, induce delayed onset of muscle soreness (DOMS), electric pain measurement |
| flupirtine intravenous | Active comparator | Drug: 100 mg flupirtine intravenous, Procedure: induce delayed onset of muscle soreness (DOMS), Procedure: electric pain measurement100 mg flupirtine intravenous, pharmacokinetics of flupirtine, induce delayed onset of muscle soreness (DOMS), electric pain measurement |
| flupirtine per os steady state | Active comparator | Drug: 400 mg flupirtine per os, Procedure: electric pain measurement400 mg flupirtine per os, pharmacokinetics of flupirtine, electric pain measurement |
Who may qualify
- Ages
- 18 to 45 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult
Key inclusion criteria (6 listed)
- age: 18 - 45 years
- sex and genetics: male and female genotyped for NAT2, UGT1A1 and GSTP1
- ethnic origin: Whites
- body weight: 19 - 27 kg/m²
- good health as evidenced by the results of the clinical examination, ECG, and the laboratory check-up, which are judged by the clinical investigator not to differ in a clinical relevant way from the normal state
Key exclusion criteria (26 listed)
- existing cardiac or hematological diseases and/or pathological findings which might interfere with safety, pharmacodynamic effect and/or pharmacokinetics of the study drug
- existing or further obstructive lung disease (e.g. bronchial asthma)
- myasthenia gravis
- existing hepatic and renal diseases and/or pathological findings which might interfere with safety, pharmacodynamic effect and/or pharmacokinetics of the study drug
- existing gastrointestinal diseases and/or pathological findings which might interfere with safety, pharmacodynamic effect and/or pharmacokinetics of the study drug
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| 100 mg flupirtine intravenousAlso: 1 vial Kadadolon® injectAdministration of 100 mg flupirtine intravenous (3 mg solution intravenously, 1 vial Kadadolon® inject) | Drug | flupirtine intravenous |
| 100 mg flupirtine per osAlso: 1 capsule Kadadolon®Administration of 100 mg flupirtine per os (1 capsule Kadadolon®) | Drug | flupirtine per os single dose |
| 400 mg flupirtine per osAlso: 1 Kadadolon® S long retard tabletAdministration of 400 mg flupirtine (1 Kadadolon® S long retard tablet) | Drug | flupirtine per os steady state |
| induce delayed onset of muscle soreness (DOMS)The DOMS exercise protocol consists of two sets of 50 concentric/eccentric contractions of the calf muscles of one leg with a rest of 5 min in-between. The exercise is performed 22-26 h prior to medication. For pain measurements, muscle pain is stimulated by standing on tiptoes of one leg for 30 s, which requires a constriction of the affected calf muscles. The other leg is lifted and the subjects are allowed to hold on to a table to keep their balance. The pain intensity during this stimulation is then rated by means of a 10 cm visual analogue scale (VAS). The VAS is extended from "no pain" to "intolerable pain" with a precision of 1 mm. The stimulation is repeated with the other leg. The sequence of the legs is chosen randomly. | Procedure or surgery | flupirtine intravenous, flupirtine per os single dose |
| electric pain measurementThe method has been described to be sensitive to quantify analgesic opioid effects. Painful 5 Hz sine waves electrical stimuli (increase of intensity 0.2 mA/s, from 0 to 20 mA), which predominantly activate C-fibres, will be applied via two gold electrodes placed on the medial and lateral side of the distal phalangeal joint (middle finger of the left hand as default-testing site). During testing, subjects keep a button continuously pressed until they find the pain intolerably and interrupt the current by releasing the button. The electrical current at which this occurred is defined as pain tolerance, the target parameter of this pain model. Each value of pain tolerance is the median of five subsequent measurements obtained at an interval of 1 min. | Procedure or surgery | flupirtine intravenous, flupirtine per os single dose, flupirtine per os steady state |
Primary outcome
bioavailability (F)
Time frame: before and 0.5,1,1.5,2,2.5,3,3.5,4,5,6,8,10,12,16,24,48,72,96,120 h after administration of study medication
ratio of the area under the concentration time curve after oral to intravenous administration of study medication
delayed onset of muscle soreness (DOMS)
Time frame: before and 2, 4, 6, 8 h after study medication
For pain measurements, muscle pain is stimulated by standing on tiptoes of one leg for 30 s, which requires a constriction of the affected calf muscles. The other leg is lifted and the subjects are allowed to hold on to a table to keep their balance. The pain intensity during this stimulation is then rated by means of a 10 cm visual analogue scale (VAS). The VAS is extended from "no pain" to "intolerable pain" with a precision of 1 mm.
electric pain threshold
Time frame: before and 2, 4, 6, 8 h (and 10, 12 h on study day 8) after study medication and on study days 1,2,3,4,5,6,7
A painful 5 Hz sine waves electrical stimuli (increase of intensity 0.2 mA/s, from 0 to 20 mA), will be applied via two gold electrodes placed on the medial and lateral side of the distal phalangeal joint (middle finger of the left hand as default-testing site). During testing, subjects keep a button continuously pressed until they find the pain intolerably and interrupt the current by releasing the button. The electrical current at which this occurred is defined as pain tolerance, the target parameter of this pain model. Each value of pain tolerance is the median of five subsequent measurements obtained at an interval of 1 min.
2 secondary outcomes
amount of excretion (Ae) in urine
Time frame: in 24 h intervals for 3 days
amount of excretion (Ae) of feces
Time frame: 5 day sampling period
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 30 Aug 2012.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
The record lists no contact. Use the official record to reach the sponsor.
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 1 study testing 100 mg flupirtine intravenous, 100 mg flupirtine per os and 400 mg flupirtine per os in people with Pain and Pharmacokinetics, run by University Medicine Greifswald at 1 site in Germany.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 6 inclusion and 26 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 30 Aug 2012. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Germany. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 1 studies test a treatment in a small group of people for the first time or in a new way, mainly to check safety and find the right dose.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
bioavailability (F) (time frame: before and 0.5,1,1.5,2,2.5,3,3.5,4,5,6,8,10,12,16,24,48,72,96,120 h after administration of study medication). The study lists 3 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 30 Aug 2012.