This page shows what was measured, who it was measured in, and what that does not settle.
What Erlosamide does in the body
The other is slow, building over seconds when a cell has been depolarised for a while.
A sodium pore in a nerve membrane has two ways of switching off. One is fast, over milliseconds, and it is what most older seizure drugs grab hold of. Lacosamide works on the slow one: it pushes channels that have been active for some time into the unavailable state and keeps them there. The practical consequence is that it acts most on tissue that has been over-excited for a while, and least on tissue behaving normally.
Why people take it. Focal epilepsy, and added-on treatment for generalised tonic-clonic seizures
What happened in people
Six-month seizure freedom of 90% against 91% on controlled-release carbamazepine in 888 newly diagnosed adults, meeting pre-defined non-inferiority criteria
✎ Source-linked record
Where this came from
A person wrote this into the record with the study named beside it. No reviewer has signed it off.
The recorded finding that sits closest to something a person would notice. Written into the record, not signed off, and it carries no population or interval.
That lacosamide works where other sodium-channel blockers have failed: no trial stratified by prior sodium-channel-blocker failure, and the head-to-head trial enrolled patients who had failed nothing
Where it acts
Axonal membrane of cortical neurons, acting on the slow-inactivated state of voltage-gated sodium channels
Kind of result
The kind of result is not recorded
Supervision
RNAWiki has not recorded a supervision or regulatory status for this substance.
What the registries record it as
The substance registry classes this as chemical.
FDA substance registry · 563KS2PQY5 · read 2026-08-29
Its recorded molecular formula is C13H18N2O3, weighing 250.30.
US prescribing information · 7ed5cebe-470e-48a4-86ec-2ce79cc32688 · read 2026-08-30
Where each sentence above came from
A person wrote this explanation into the record, with the studies named in the path below.
The recorded use, written for a reader without medical training. Not signed off.
A limit recorded against this substance. Not signed off as a reviewed claim.
The four opening statements run to 120 words.
Words this page uses
Four words worth knowing first
Chosen from what this page shows, with each one explained before the word it depends on.
Comparator
A comparator is whatever the treatment was measured against.
A picture of it, and where the picture fails
It is like the other runner in a race.
Where that stops being true. A race has one winner. A study can show both arms improved.
What people get wrong. Results are read without asking what the other group got. Beating nothing is not beating a treatment.
The control condition against which the experimental intervention is assessed.
Randomisation
Randomisation means chance decides who gets which treatment.
A picture of it, and where the picture fails
It is like a coin toss deciding the groups.
Where that stops being true. A coin toss is fair once. Fairness here comes from doing it for everyone.
What people get wrong. It is thought to make groups identical. It makes them similar on average, including on things nobody measured.
Allocation of participants to arms by a chance process, so that unmeasured factors are balanced in expectation.
Absolute difference
An absolute difference is how many more people in a hundred were affected.
A picture of it, and where the picture fails
It is like counting heads in two rooms of a hundred.
Where that stops being true. Heads are easy to count. Study results carry a margin of error too.
What people get wrong. It is confused with a percentage change, which can look far larger.
The arithmetic difference in event rates between arms.
Confidence interval
A confidence interval is the range the true answer is likely to sit in.
A picture of it, and where the picture fails
It is like a weather forecast giving a range rather than one number.
Where that stops being true. A forecast range covers tomorrow. This one covers what the study could resolve.
What people get wrong. The middle number is read as the answer. A range crossing zero means no change is still possible.
An interval estimate that would contain the true parameter in a stated proportion of repeated studies.
What happened in people◇Read from sources, not yet reviewed
What happened in people
Each card is one study: the exact question it asked, who was in it, and whether it showed what it set out to show.
Proportion of patients free from seizures for 6 consecutive months after stabilisation at the last assessed dose
✓ The study showed what it set out to show
Who was studied
Lacosamide versus carbamazepine-CR in newly diagnosed epilepsy (NCT01243177)
Kaplan-Meier 6-month seizure freedom 90% on lacosamide against 91% on carbamazepine-CR; absolute difference -1.3% (95% CI -5.5 to 2.8), within the pre-defined -12% absolute and -20% relative non-inferiority criteria
Repeated elsewhere
Unreplicated
What this does not prove. Meeting one endpoint in one population does not carry to other goals or other people.
The limits of this study, and where it came from
Main limit. Withdrawal for treatment-emergent adverse events was 11% on lacosamide and 16% on carbamazepine-CR. The trial was funded by UCB Pharma, the manufacturer of lacosamide.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral tablet, oral solution, extended-release capsule and intravenous infusion
Interval reported. 95% CI -5
Written into the record, not signed off as a reviewed claim.
Percentage of patients meeting pre-specified exit criteria during the maintenance phase, against a pooled historical control
✓ The study showed what it set out to show
Who was studied
Monotherapy Study 1 (label Clinical Studies 14.1)
How many people
425
Study design
Historical-control multicentre randomised trial, blinded between two lacosamide doses
Compared against
Not recorded for this study
Kind of result
A number that stands in for health
What was found
30% met at least one exit criterion at 400 mg/day (95% CI 25% to 36%); the upper limit of 36% fell below the 65% threshold derived from historical sub-therapeutic control groups
Repeated elsewhere
Partially Replicated
What this does not prove. Meeting one endpoint in one population does not carry to other goals or other people.
The limits of this study, and where it came from
Main limit. There is no concurrent comparator. The benchmark is a pooled analysis of control groups from eight earlier studies in which patients received a deliberately sub-therapeutic dose of a different drug.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral tablet, oral solution, extended-release capsule and intravenous infusion
Interval reported. 95% CI 25% to 36%); the upper limit of 36% fell below the 65% threshold derived from historical sub-therapeutic control groups
Written into the record, not signed off as a reviewed claim.
Hazard ratio 0.548 (95% CI 0.381 to 0.788), P=0.001, a 45.2% risk reduction; 24-week PGTC seizure freedom 31.3% against 17.2%, adjusted difference 14.1% (3.2 to 25.1), P=0.011
Repeated elsewhere
Unreplicated
What this does not prove. Meeting one endpoint in one population does not carry to other goals or other people.
The limits of this study, and where it came from
Main limit. No limitation is recorded for this study.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral tablet, oral solution, extended-release capsule and intravenous infusion
Interval reported. 95% CI 0
Written into the record, not signed off as a reviewed claim.
Three 12-week randomised double-blind placebo-controlled multicentre trials
Compared against
A dummy treatment
Kind of result
A number that stands in for health
What was found
Statistically significant at 200 mg/day in Study 4, at 400 mg/day in all three studies, and at 600 mg/day in Studies 2 and 3; the label reports the comparison graphically
Repeated elsewhere
Replicated
What this does not prove. Meeting one endpoint in one population does not carry to other goals or other people.
The limits of this study, and where it came from
Main limit. The pooled safety population for the cardiac analysis was 944 lacosamide and 364 placebo patients, in whom asymptomatic first-degree AV block occurred in 0.4% and 0% respectively.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral tablet, oral solution, extended-release capsule and intravenous infusion
Interval reported. Not recorded in this summary
Written into the record, not signed off as a reviewed claim.
RNAWiki holds 4 written-up human studies for this substance, each with the question it asked.
How we know it
Each card names the study, the number of people and what the study set out to measure.
What this does not prove
These summaries were written by a person and have not been signed off as reviewed claims.
Why it matters
A study that failed is as informative as one that worked, and both are here.
What we still do not know
No reviewed claim exists, so no exact population, effect size or interval is published yet.
What it changes in the body◇Read from sources, not yet reviewed
The path through the body
From what a person takes to what changes. A solid line is a step measured in people. A dashed line is a step nobody has measured that way.
Start
Erlosamide
What a person takes: Oral tablet, oral solution, extended-release capsule and intravenous infusion.
The measurement behind this step
The intravenous form is bioequivalent to the oral, so a person can be moved between them without recalculating exposure, and that is the main reason lacosamide entered hospital practice quickly. The label notes one case of profound bradycardia during a 15-minute infusion of 150 mg, and infusion rate is therefore not a neutral choice. The extended-release capsule Motpoly XR is a separate FDA application.
Getting in
Swallowed or infused, with almost complete bioavailability either way
Absorption is essentially complete and food does not matter. The intravenous form delivers the same exposure, which is why a person in hospital can be switched between routes without recalculating.
╌╌Described, with no measurement named. No measurement is named for this step, so it is drawn as an unconfirmed link.
The measurement behind this step
Oral bioavailability approaches 100%, protein binding is under 15%, and the intravenous form is bioequivalent to the oral. Metabolism to the inactive O-desmethyl metabolite involves CYP2C19 among others, but the drug is neither a significant inducer nor a significant inhibitor, so the interaction burden is minimal.
The molecule crosses into brain tissue and reaches the outer membrane of nerve cell axons, where sodium pores sit.
╌╌Described, with no measurement named. No measurement is named for this step, so it is drawn as an unconfirmed link.
The measurement behind this step
Distribution is rapid with a volume of distribution close to total body water. The relevant compartment is the axonal membrane of cortical neurons; unlike topiramate and zonisamide, lacosamide has no carbonic anhydrase activity, so it produces no renal, ocular or sweat gland effects.
Sodium pores have two ways of becoming unavailable: one that happens in milliseconds and one that builds over seconds. Older drugs use the fast route. This one uses the slow route, which means it acts on tissue that has been over-excited for a while.
╌╌Measured in animals. A result in animals says what to test next. It does not say what happens in people.
The measurement behind this step
The label states that in vitro electrophysiological studies show lacosamide selectively enhances slow inactivation of voltage-gated sodium channels, stabilising hyperexcitable neuronal membranes and inhibiting repetitive neuronal firing, and that the precise mechanism in humans remains to be fully elucidated. Detecting the effect requires conditioning prepulses lasting seconds; standard fast-inactivation protocols largely miss it.
The pool of available channels shrinks where firing has been sustained
Tissue that has been quietly behaving keeps most of its pores. Tissue that has been depolarised for seconds loses a growing share of them, so it cannot keep a burst going.
──Measured in people. Written by a person from the study named beside the step. Not signed off as a reviewed claim.
The measurement behind this step
Enhancement of slow inactivation reduces the available channel pool in a use- and time-dependent way without the acute effect on single action potentials that fast-inactivation blockers produce. The clinical corollary the label supports is inhibition of repetitive firing; the corollary it does not support is a specific advantage in patients who have failed fast-inactivation drugs.
Seizure freedom equal to carbamazepine, and 45% less risk of a second convulsion
In newly diagnosed adults, 90% were seizure-free at six months against 91% on carbamazepine. In generalised epilepsy, the risk of a second convulsive seizure fell by 45% against placebo.
──Measured in people. Written by a person from the study named beside the step. Not signed off as a reviewed claim.
The measurement behind this step
Efficacy is established against placebo in three adjunctive partial-onset trials, against placebo in one primary generalised tonic-clonic trial (HR 0.548, 95% CI 0.381 to 0.788), and against controlled-release carbamazepine on a pre-specified non-inferiority margin in 888 newly diagnosed adults. The monotherapy indication itself was originally granted against a historical control rather than an active one.
No suggested links are held for this record, so nothing is hidden from this path.
What we know
The record describes 5 steps from taking it to an effect in a person.
How we know it
Each step names the study behind it in the technical detail beside it.
What this does not prove
A change inside the body is a reason to look. It is not a result in a person.
Why it matters
A reader can see exactly where the chain stops being measured in people.
What we still do not know
No reviewed claim binds any of these steps to a named population.
What is missing or unclear◇Read from sources, not yet reviewed
Were people like you studied?
RNAWiki cannot tell whether a study fits you. It can show who was in it, and where the result stops carrying.
Who was studied
People similar to this profile were included.
People with focal epilepsy from one month of age, and people with generalised tonic-clonic seizures as an add-on. The intravenous form is widely used in hospital when someone cannot take tablets.
Who is missing from the studies
Which groups were under-represented in the studies has not been recorded for this substance. Pregnancy, breastfeeding, children, older adults, and people with liver or kidney conditions are commonly excluded from trials; nothing here says whether they were.
What the label states about particular groups
On pediatric, the label states: “Safety and effectiveness in pediatric patients below 1 month of age have not been established.”
US prescribing information · 7ed5cebe-470e-48a4-86ec-2ce79cc32688 · read 2026-08-30
On older people, the label states: “There were insufficient numbers of elderly patients enrolled in partial -onset seizure trials (n=18) to adequately determine whether they respond differently from younger patients.”
US prescribing information · 7ed5cebe-470e-48a4-86ec-2ce79cc32688 · read 2026-08-30
On people who are pregnant, the label states: “Exposure Registry There is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to antiepileptic drugs (AEDs), such as lacosamide, during pregnancy.”
US prescribing information · 7ed5cebe-470e-48a4-86ec-2ce79cc32688 · read 2026-08-30
On people who are breastfeeding, the label states: “Risk Summary Data from published literature indicate that lacosamide is present in human milk.”
US prescribing information · 7ed5cebe-470e-48a4-86ec-2ce79cc32688 · read 2026-08-30
On people with reduced liver function, the label states: “For adult and pediatric patients with mild to moderate hepatic impairment, a reduction of 25% of the maximum dosage is recommended.”
US prescribing information · 7ed5cebe-470e-48a4-86ec-2ce79cc32688 · read 2026-08-30
On people with reduced kidney function, the label states: “No dose adjustment is necessary in patients with mild to moderate renal impairment (CL CR ≥30 mL/min).”
US prescribing information · 7ed5cebe-470e-48a4-86ec-2ce79cc32688 · read 2026-08-30
Where the result stopped carrying
The CRMP-2 target was searched for by radioligand binding and by surface plasmon resonance and was not detected by either; the calcium-channel consequence attributed to it was also absent
Standard fast-inactivation electrophysiology protocols, the ones built around older drugs, largely miss this drug effect and would have under-rated it
The monotherapy indication was originally granted without a concurrent active comparator; the comparison that mattered arrived nine years later
This is a scope explorer, not a diagnosis engine.
It shows who was studied so you can see whether people similar to you were included.
RNAWiki cannot tell whether a study fits you. It can show who was in it.
What it would be like to take◇Read from sources, not yet reviewed
Why it might seem to do nothing
A real effect and a noticed effect are different things. These are the recorded reasons the two come apart.
It was studied in different people
The people in the studies were not much like the reader.
On this record: Which groups were under-represented in the studies has not been recorded for this substance. Pregnancy, breastfeeding, children, older adults, and people with liver or kidney conditions are commonly excluded from trials; nothing here says whether they were.
The evidence may simply be wrong
Small early studies often do not hold up.
On this record: RNAWiki has not yet published a reviewed conclusion for this use.
Other reasons RNAWiki checked and found nothing for (11)
It was studied for a different goal
The studies measured something else entirely. Nothing in this record points to this reason.
A different form was studied
The studied form is not the form on the shelf. Nothing in this record points to this reason.
There was nothing to correct
Where a level is already normal, topping it up may change nothing. Nothing in this record points to this reason.
Something else had to happen too
In the studies it was paired with training, a diet or another treatment. Nothing in this record points to this reason.
The change is too small to feel
A real change can still sit below what a person notices. Nothing in this record points to this reason.
Day-to-day swing hides it
Sleep, food, stress and time of day move most numbers more than this would. Nothing in this record points to this reason.
Not enough time yet
The studies ran longer than the person has waited. Nothing in this record points to this reason.
It was not taken as studied
Missed days change the result, and studies count them. Nothing in this record points to this reason.
Something else changed at the same time
Two changes at once cannot be told apart afterwards. Nothing in this record points to this reason.
The product may not be what it says
Contents of a sold product are not always what the label states. Nothing in this record points to this reason.
No recorded reason
RNAWiki has nothing stored that would explain it. Nothing in this record points to this reason.
None of these is a reason to take more. Taking more is not a step this page ever suggests.
What it would be like to take◇Read from sources, not yet reviewed
What taking it involves
The recorded facts about getting hold of it and using it. Nothing here is a suggestion about what you should do.
How it is supplied
Given by a clinician
❝ Quoted from a source
Where this came from
Copied from a source RNAWiki stored, with the source named.
Read from the recorded approval status.
No source is stored against this line.
Form and route
Oral tablet, oral solution, extended-release capsule and intravenous infusion
✎ Source-linked record
Where this came from
A person wrote this into the record with the study named beside it. No reviewer has signed it off.
The form and route recorded on this substance.
No source is stored against this line.
Who oversees it
RNAWiki has not recorded a supervision or regulatory status for this substance.
❝ Quoted from a source
Where this came from
Copied from a source RNAWiki stored, with the source named.
No register row and no identity class settled the question.
No source is stored against this line.
What is in the pack
The intravenous form is bioequivalent to the oral, so a person can be moved between them without recalculating exposure, and that is the main reason lacosamide entered hospital practice quickly. The label notes one case of profound bradycardia during a 15-minute infusion of 150 mg, and infusion rate is therefore not a neutral choice. The extended-release capsule Motpoly XR is a separate FDA application.
✎ Source-linked record
Where this came from
A person wrote this into the record with the study named beside it. No reviewer has signed it off.
Recorded notes on how this is sold and what that means for what is in the pack.
No source is stored against this line.
Where it is registered
Regulatory records are listed in the technical disclosure at the foot of this page.
# Counted from records
Where this came from
A count of rows RNAWiki holds. It describes our records, not your body.
Register entries are stored per jurisdiction and shown with their dates.
No source is stored against this line.
Why people stop
Not recorded.
∅ Nothing recorded
Where this came from
RNAWiki holds nothing here and says so rather than guessing.
No record of why people stopped taking it is stored for this substance.
No source is stored against this line.
What it would be like to take◇Read from sources, not yet reviewed
What can go wrong
Sorted by where each line came from. A regulator's label and a report somebody sent in are not the same kind of fact.
·Worth asking a clinician aboutWritten into the record from the studies named on this page
No boxed warning. The distinctive risk is cardiac: dose-dependent PR interval prolongation, asymptomatic first-degree AV block in 0.4% against 0% on placebo, and post-marketing reports of bradycardia, AV block and ventricular tachyarrhythmia rarely resulting in asystole, cardiac arrest and death, mostly in people with a predisposing condition or an interacting drug. An ECG before starting and after titration is recommended in those patients. Dizziness, ataxia and syncope have their own warning sections and are the commonest reasons for withdrawal. DRESS and multi-organ hypersensitivity are listed. Abrupt withdrawal risks increased seizure frequency. It is a Schedule V controlled substance on the strength of a supratherapeutic euphoria signal. The class-wide suicidality warning applies.
Nobody counted how many people took this and were fine, so this cannot be turned into a rate.
Over a long time. No completed tested study window is recorded, so long-term effects are not established by the registry record.
Groups the studies covered thinly. Which groups were under-represented in the studies has not been recorded for this substance. Pregnancy, breastfeeding, children, older adults, and people with liver or kidney conditions are commonly excluded from trials; nothing here says whether they were.
What is missing or unclear◇Read from sources, not yet reviewed
Does the exact form matter?
Evidence belongs to the exact thing that was tested. A different salt, a different mixture or a different preparation is a different question.
The form that was studied
Oral tablet, oral solution, extended-release capsule and intravenous infusion
✎ Source-linked record
Where this came from
A person wrote this into the record with the study named beside it. No reviewer has signed it off.
The form used in the studies cited on this page.
No source is stored against this line.
What is sold
The label notes one case of profound bradycardia during a 15-minute infusion of 150 mg, and infusion rate is therefore not a neutral choice. The extended-release capsule Motpoly XR is a separate FDA application.
✎ Source-linked record
Where this came from
A person wrote this into the record with the study named beside it. No reviewer has signed it off.
Recorded notes on which forms are sold and how they compare.
No source is stored against this line.
What is recorded as being sold
196 products list this as an active ingredient in the United States drug directory. 196 of them contain it and nothing else.
FDA National Drug Code directory · 71921-221 · read 2026-08-29
They are sold as capsule, extended release, injection, injection, solution, powder, powder, for solution and solution, taken intravenous and oral.
FDA National Drug Code directory · 71921-221 · read 2026-08-29
The regulator's established pharmacologic class for it is decreased central nervous system disorganized electrical activity [pe].
FDA National Drug Code directory · 71921-221 · read 2026-08-29
76 published labels name it as an active ingredient. 76 of them describe this substance alone, which is where its own label text on this page comes from.
US prescribing information · 7ed5cebe-470e-48a4-86ec-2ce79cc32688 · read 2026-08-29
Those labels are classed as human prescription drug.
US prescribing information · 7ed5cebe-470e-48a4-86ec-2ce79cc32688 · read 2026-08-29
Lacosamide is oral at 3 DOSAGE FORMS AND STRENGTHS Lacosamide Tablets, USP 50 mg: White to off white, oval film-coated tablets, debossed with "U" on one side and "364" on the other. 100 mg: Green oval film-coated tablets, debossed with "U" o…, recorded as fda label in effect 2024-09-17 in the United States.
US prescribing information · 7ed5cebe-470e-48a4-86ec-2ce79cc32688 · read 2026-08-30
Recorded price in US: 0.08203 USD per one millilitre, across 15 priced products whose strengths and pack forms differ, as of 2026-08-26, paid by retail pharmacies buying the product, as surveyed by the Centers for Medicare & Medicaid Services. It is not a list price, an insurance price, or what anyone pays at a counter..
Recorded source · 2026-08-26 · read 2026-08-28
Recorded price in US: 0.11527–0.24661 USD per one unit as the pricing file counts it — a tablet, capsule, patch or single item, across 62 priced products whose strengths and pack forms differ, as of 2026-08-26, paid by retail pharmacies buying the product, as surveyed by the Centers for Medicare & Medicaid Services. It is not a list price, an insurance price, or what anyone pays at a counter..
Recorded source · 2026-08-26 · read 2026-08-28
Evidence carries across two names for one substance. It does not carry across a salt, a mirror form or a mixture.
What it would be like to take◇Read from sources, not yet reviewed
What you could measure
This one is decided with a clinician, so this section holds questions to ask rather than a plan to run.
RNAWiki could not confidently classify this substance, so no self-experiment plan is offered.
Questions worth asking
Which of the trials of Erlosamide studied people like me?
What was measured, and for how long?
Was the result a laboratory value or a health outcome?
What would we watch for, and when would we stop?
Tracking can show whether something changed for you. It cannot show what caused it.
RNAWiki records evidence. It does not say whether this substance is right for you.
What is missing or unclear◇Read from sources, not yet reviewed
Claims that go past the evidence
Things said about this substance that sound reasonable, and the exact step that is missing between the evidence and the claim.
✗Goes past the evidence
That lacosamide works where other sodium-channel blockers have failed: no trial stratified by prior sodium-channel-blocker failure, and the head-to-head trial enrolled patients who had failed nothing
Why it sounds right. It follows from something real on this page: a body step, an animal result or a related finding.
The missing step. Nobody measured this in people for this use, or the study that did measure it did not show it.
What would change this
A study in people, for this exact use, measuring this exact thing, that a reviewer signs off.
RNAWiki has not yet published a reviewed conclusion for this use.
✗Goes past the evidence
That combining lacosamide with a fast-inactivation sodium-channel blocker is mechanistically rational: the reasoning is plausible and the clinical test has not been done
Why it sounds right. It follows from something real on this page: a body step, an animal result or a related finding.
The missing step. Nobody measured this in people for this use, or the study that did measure it did not show it.
What would change this
A study in people, for this exact use, measuring this exact thing, that a reviewer signs off.
RNAWiki has not yet published a reviewed conclusion for this use.
✗Goes past the evidence
That the original monotherapy approval demonstrated efficacy against an alternative treatment, when the comparator was a historical pool of sub-therapeutic control groups
Why it sounds right. It follows from something real on this page: a body step, an animal result or a related finding.
The missing step. Nobody measured this in people for this use, or the study that did measure it did not show it.
What would change this
A study in people, for this exact use, measuring this exact thing, that a reviewer signs off.
RNAWiki has not yet published a reviewed conclusion for this use.
✗Goes past the evidence
That the dual CRMP-2 mechanism contributes anything, a claim that circulated for years and did not survive being tested
Why it sounds right. It follows from something real on this page: a body step, an animal result or a related finding.
The missing step. Nobody measured this in people for this use, or the study that did measure it did not show it.
What would change this
A study in people, for this exact use, measuring this exact thing, that a reviewer signs off.
RNAWiki has not yet published a reviewed conclusion for this use.
What is missing or unclear◇Read from sources, not yet reviewed
What nobody knows yet
Open questions, each with why it is open and what would close it.
Missing populations
Which groups were under-represented in the studies has not been recorded.
Why it matters. Recorded by the evidence model as a gap on this record.
What would answer it
A study that measures it, and a reviewer to sign it off.
Last checked 2026-09-04. Searched: The sources listed in the receipts at the foot of this page.
Missing long-term data
No completed tested study window is recorded.
Why it matters. Recorded by the evidence model as a gap on this record.
What would answer it
A study that measures it, and a reviewer to sign it off.
Last checked 2026-09-04. Searched: The sources listed in the receipts at the foot of this page.
No reviewed conclusion
RNAWiki has not yet published a reviewed conclusion for this use.
Why it matters. Recorded by the evidence model as a gap on this record.
What would answer it
A study that measures it, and a reviewer to sign it off.
Last checked 2026-09-04. Searched: The sources listed in the receipts at the foot of this page.
Missing interaction studies
No interaction was found in the registers checked. Not finding one is not the same as showing there is none.
Why it matters. Recorded by the evidence model as a gap on this record.
What would answer it
A study that measures it, and a reviewer to sign it off.
Last checked 2026-09-04. Searched: The sources listed in the receipts at the foot of this page.
Formulation uncertainty
Several salts, forms or products of Erlosamide are recorded. Results from one form may not transfer to another.
Why it matters. Recorded by the evidence model as a gap on this record.
What would answer it
A study that measures it, and a reviewer to sign it off.
Last checked 2026-09-04. Searched: The sources listed in the receipts at the foot of this page.
Mechanism not reviewed
No reviewed mechanism story exists for this substance.
Why it matters. Recorded by the evidence model as a gap on this record.
What would answer it
A study that measures it, and a reviewer to sign it off.
Last checked 2026-09-04. Searched: The sources listed in the receipts at the foot of this page.
What happened in people◇Read from sources, not yet reviewed
Check any of this yourself
Every line above traced back to the study it came from. This is the technical layer, and the vocabulary changes here.
Every line above can be traced to the study named beside it. Follow the link and read it.
Non-inferior to controlled-release carbamazepine in 888 newly diagnosed adults
In plain words
A double-blind trial gave newly diagnosed adults either lacosamide or the older standard, carbamazepine, and counted how many stayed seizure-free for six months. Ninety percent did on lacosamide and 91% on carbamazepine, which met the trial pre-set definition of no worse.
What was measured
Proportion of patients free from seizures for 6 consecutive months after stabilisation at the last assessed dose
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
Baulac and colleagues randomised 888 patients with newly diagnosed epilepsy, double-blind, to lacosamide starting at 100 mg/day or carbamazepine-CR starting at 200 mg/day, with escalation to the next target level after any seizure and a fresh six-month assessment period each time. The full analysis set was 444 and 442; the per-protocol set 408 and 397. Six months of seizure freedom was completed by 327 (74%) on lacosamide and 308 (70%) on carbamazepine-CR. Kaplan-Meier estimated six-month seizure freedom was 90% against 91%, an absolute difference of -1.3% (95% CI -5.5 to 2.8) and a relative difference of -6.0%, against pre-defined non-inferiority criteria of -12% absolute and -20% relative. Per-protocol estimates were 92% and 93% (-1.3%, -5.3 to 2.7). Treatment-emergent adverse events occurred in 74% and 75%; serious ones in 7% and 10%; withdrawal for adverse events in 11% and 16%. The trial was funded by UCB Pharma, which is a fact about who paid rather than a criticism of the design, and the design is the strongest of any registration programme on these pages.
Written into the record, not signed off as a reviewed claim
The second mechanism was looked for with two methods and was not there
In plain words
Lacosamide was introduced as a drug with two targets: sodium channels and a protein called CRMP-2. In 2012 two independent binding techniques were used to look for that second interaction. Neither found it, and the claim quietly left the label.
What was measured
That lacosamide has a dual mechanism involving CRMP-2. Two orthogonal binding methods found no specific interaction, and the label no longer makes the claim.
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
Early preclinical work proposed that lacosamide had an additional mode of action through binding to collapsin response mediator protein 2, and the dual-mechanism description appeared widely in reviews and in early prescribing information. Errington and colleagues tested it directly using radioligand binding with tritiated lacosamide at free concentrations of 100 to 1,450 nM and surface plasmon resonance over 0.39 to 100 micromolar, against both isolated and membrane-bound human CRMP-2 expressed in mammalian cells and in bacteria. No specific binding was observed by either method, and the authors noted that both techniques were well suited to detect binding in the micromolar range. Separately, Wang and Khanna showed that lacosamide did not affect N-type, P/Q-type or L-type calcium currents, including N-type currents augmented by CRMP-2 expression, removing the proposed downstream consequence as well. The current United States label describes only selective enhancement of slow inactivation of voltage-gated sodium channels and states that the precise mechanism remains to be fully elucidated.
Written into the record, not signed off as a reviewed claim
The monotherapy licence was granted against a historical control, not a randomised one
In plain words
The trial that established lacosamide as a stand-alone drug randomised 425 patients between two doses of lacosamide and then compared them with a pooled group of patients from eight earlier studies who had been given a deliberately ineffective dose of a different drug.
What was measured
Percentage of patients meeting pre-specified exit criteria, against a 65% threshold derived from pooled historical sub-therapeutic control groups
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
Study 1 was a historical-control, multicentre, randomised trial in 425 patients aged 16 to 70 with partial-onset seizures on 1 or 2 existing drugs. After an 8-week baseline and 3-week titration, patients entered a 16-week maintenance phase in which background drugs were withdrawn over 6 weeks and lacosamide continued alone for 10 weeks. Randomisation was 3 to 1 between lacosamide 400 mg/day and 300 mg/day, with treatment assignment blinded. The comparison was not between those two arms: it was against a pooled analysis of the control groups from eight studies of similar design that had used a sub-therapeutic dose of an antiepileptic drug. Superiority was declared if the upper limit of the two-sided 95% confidence interval for the percentage meeting exit criteria fell below a 65% lower prediction limit derived from that pooled historical data. For lacosamide 400 mg/day the estimate was 30% (95% CI 25% to 36%), and 36% is below 65%, so the criterion was met. What that establishes is that lacosamide performs better than a group of historical patients on a deliberately inadequate dose of something else. The Baulac trial, published nine years later, is what establishes performance against a real comparator.
Source
Lacosamide United States prescribing information, Clinical Studies 14.1, Study 1 (openFDA drug label endpoint)
Role in the trial
Not matched to a registered study
Identity check
no open identity hold
Audit mark
caution
Review state
Written into the record, not signed off as a reviewed claim
Generalised tonic-clonic seizures: 45% lower risk of a second one
In plain words
In 242 patients with generalised epilepsy having convulsive seizures, adding lacosamide cut the risk of a second such seizure over 24 weeks by 45%, and 31.3% went the whole period without one against 17.2% on placebo.
What was measured
Time to second primary generalised tonic-clonic seizure over 24 weeks, and 24-week seizure freedom
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
Study 5 was a 24-week double-blind randomised placebo-controlled parallel-group trial in patients aged 4 and over with idiopathic generalised epilepsy having primary generalised tonic-clonic seizures, on stable doses of 1 to 3 anti-seizure drugs and with at least 3 documented PGTC seizures across a 16-week combined baseline. Randomisation was 1:1 to lacosamide (n=121) or placebo (n=121), with a fixed-dose regimen targeting 400 mg/day in patients weighing 50 kg or more. In the modified full analysis set (118 and 121), time to second PGTC seizure favoured lacosamide with a hazard ratio of 0.548 (95% CI 0.381 to 0.788, p=0.001), a 45.2% risk reduction. Adjusted Kaplan-Meier estimates of 24-week freedom from PGTC seizures were 31.3% against 17.2%, an adjusted difference of 14.1% (95% CI 3.2 to 25.1, p=0.011). This is one of very few placebo-controlled results on these pages where the endpoint is a specific seizure type occurring or not, rather than a percentage change in a count.
Source
Lacosamide United States prescribing information, Clinical Studies 14.3, Study 5 (openFDA drug label endpoint)
Role in the trial
Not matched to a registered study
Identity check
no open identity hold
Audit mark
verified
Review state
Written into the record, not signed off as a reviewed claim
Adjunctive efficacy replicated across three placebo-controlled trials
In plain words
Three separate 12-week trials in adults whose seizures continued on up to three other drugs all found a significant reduction against placebo, at 400 mg a day in every one of them.
What was measured
Reduction in 28-day partial-onset seizure frequency from baseline to maintenance phase, against placebo, by dose
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
Studies 2, 3 and 4 were 12-week randomised double-blind placebo-controlled multicentre trials in adults with partial-onset seizures inadequately controlled on 1 to 3 concomitant drugs, requiring an average of at least 4 seizures per 28 days over an 8-week baseline with no seizure-free period exceeding 21 days. Mean duration of epilepsy was 24 years and median baseline seizure frequency ranged from 10 to 17 per 28 days; 84% were taking 2 to 3 concomitant drugs with or without vagal nerve stimulation. The primary variable was reduction in 28-day seizure frequency from baseline to the maintenance phase against placebo. A statistically significant effect was seen at 200 mg/day in Study 4, at 400 mg/day in all three studies, and at 600 mg/day in Studies 2 and 3. This is a refractory population with two decades of epilepsy behind it, which is the hardest place to show an effect and the reason the effect sizes are modest.
Source
Lacosamide United States prescribing information, Clinical Studies 14.2, Studies 2, 3 and 4 (openFDA drug label endpoint)
Role in the trial
Not matched to a registered study
Identity check
no open identity hold
Audit mark
verified
Review state
Written into the record, not signed off as a reviewed claim
It lengthens the PR interval, and post-marketing reports include cardiac arrest
In plain words
Lacosamide slows electrical conduction through the heart. In trials this was almost always harmless. After marketing, reports arrived of serious arrhythmias, some fatal, mostly in people who already had a heart problem or another drug doing the same thing.
What was measured
Incidence of asymptomatic first-degree AV block in adjunctive trials against placebo, plus post-marketing arrhythmia reports
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
Dose-dependent PR interval prolongation has been observed in adult patients and in healthy volunteers. In adjunctive trials in adults with partial-onset seizures, asymptomatic first-degree atrioventricular block occurred in 0.4% (4 of 944) of lacosamide patients and 0% (0 of 364) of placebo patients. One case of profound bradycardia occurred during a 15-minute infusion of 150 mg. Post-marketing reports include bradycardia, AV block and ventricular tachyarrhythmia, rarely resulting in asystole, cardiac arrest and death, occurring with both oral and intravenous routes and at prescribed doses as well as in overdose; most but not all occurred in patients with underlying proarrhythmic conditions or on concomitant medications affecting cardiac conduction. The label recommends an ECG before starting and after titration to steady state in those patients. The gap between a 0.4% asymptomatic finding in trials and fatal post-marketing reports is the standard shape of a rare cardiac signal: trials exclude the people at risk, and marketing does not.
Source
Lacosamide United States prescribing information, Warnings and Precautions 5.3 (openFDA drug label endpoint)
Role in the trial
Not matched to a registered study
Identity check
no open identity hold
Audit mark
caution
Review state
Written into the record, not signed off as a reviewed claim
Schedule V, on a euphoria score that matched a benzodiazepine
In plain words
At twice the recommended daily dose in a single sitting, lacosamide produced euphoria that was statistically indistinguishable from alprazolam. That result, not any pattern of misuse, is why it is a controlled substance.
What was measured
Euphoria-type subjective responses at supratherapeutic single doses against placebo and against alprazolam
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
In a human abuse potential study, single doses of 200 mg, equal to the maximum single dose, and 800 mg, equal to twice the recommended daily maintenance dose, produced euphoria-type subjective responses that differed statistically from placebo. At 800 mg those responses were statistically indistinguishable from alprazolam, a Schedule IV drug, though of shorter duration. Euphoria was reported as an adverse event in 15% (5 of 34) at 800 mg against 0% on placebo, and in 6% (2 of 33) to 25% (3 of 12) across two pharmacokinetic studies at 300 to 800 mg against 0% on placebo. At therapeutic doses across the whole development programme, euphoria was reported in less than 1% of patients. Lacosamide is Schedule V in the United States, the least restrictive schedule.
Source
Lacosamide United States prescribing information, Drug Abuse and Dependence 9.2 (openFDA drug label endpoint)
Role in the trial
Not matched to a registered study
Identity check
no open identity hold
Audit mark
verified
Review state
Written into the record, not signed off as a reviewed claim
A different mechanism has not been shown to produce a different clinical result
In plain words
Acting on slow inactivation instead of fast is a genuine pharmacological distinction. What has not been shown is that it makes the drug work where the older ones fail, or work in someone the older ones did not help.
What was measured
That acting on slow rather than fast inactivation makes lacosamide effective where other sodium-channel blockers have failed, or makes it a rational partner for one of them
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
The slow-inactivation mechanism is well supported in cellular electrophysiology and is the reason lacosamide was missed by screening protocols built around fast inactivation. The clinical inference commonly drawn from it, that lacosamide can succeed in patients who have failed other sodium-channel blockers, is not established by any of the trials on this page. The registration programme enrolled patients refractory to 1 to 3 drugs without stratifying by whether those drugs were sodium-channel blockers, and the Baulac trial enrolled newly diagnosed patients who had failed nothing. Combining lacosamide with another sodium-channel blocker is common practice and rests on the same untested inference. The measured result is that lacosamide is as good as carbamazepine in people who have not tried either, which is a different claim.
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What is not here
7 questions this page could not answer
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What was measured, goal by goal — found nothing in the sources checked.
How close this is to real life — found nothing in the sources checked.
Felt, measured, or meaningful — found nothing in the sources checked.
How long anything takes — found nothing in the sources checked.
What it may clash with — found nothing in the sources checked.
Other ways to the same goal — found nothing in the sources checked.
What changed on this page — found nothing in the sources checked.
The record as stored
The full record, for auditing
Everything above is built from what is below. This layer keeps the technical vocabulary, record identifiers and every stored row, so a reader who wants to check the page can.
The older medicine-wide conclusion held in this record
Written for a clinical reader, and about the medicine as a whole rather than about one indication, population and set of trials. RNAWiki does not treat it as a programme conclusion and no reviewer has signed it off in that form. It is here word for word because it is what the record holds.
A sodium-channel drug that acts on slow inactivation rather than fast, which met its pre-specified non-inferiority criteria against controlled-release carbamazepine in 888 newly diagnosed adults (90% against 91% seizure-free at six months) and cut the risk of a second generalised tonic-clonic seizure by 45%, and whose originally advertised second target, CRMP-2, was searched for by two independent binding methods and not found.
Recorded evidence blocks (10)
Q1
On the Erlosamide label: indicated for what?
"Lacosamide oral solution is indicated for: Treatment of partial-onset seizures in patients 1 month of age and older ( 1.1 ) Adjunctive therapy in the treatment of primary generalized tonic-clonic seizures in patients 4 years of age and older ( 1.2 ) 1.1 Partial-Onset Seizures Lacosamide oral solution is indicated for…": indications and usage on Erlosamide's label. DailyMed label · b9a0ca8c-593c-48e8-b2a7-d30d5f6e6a9b · 2026-08-12
Q2
105 registered trials of Erlosamide — at which phases?
"Based on the outcome of the planned first interim analysis, it was decided not to continue the trial. No safety concerns were identified."; 10 of 105 registered studies
Show the evidence
Trial
NCT00485472
terminated; "Based on the outcome of the planned first interim analysis, it was decided not to continue the trial. No safety concerns were identified."
NCT01110187
terminated; "Lack of enrollement"
NCT01375374
terminated; "Slow progress despite recruitment boosting efforts e.g., expert advice obtained from leading study center Investigators; decision thus made to terminate."
NCT01724918
terminated; "Time limitation for recruitment exceeded. 72 of 90 estimated sample recruited."
NCT02342977
withdrawn; "We were unable to enroll any patients into the study."
NCT02409433
terminated; "due to slow recruitment and budgetary restraints study was prematurely terminated"
4 further recorded trials
NCT02726867
withdrawn; "No participants enrolled"
NCT03436433
terminated; "Did not enroll as planned"
NCT03777956
terminated; "COVID 19 and recruitment problems"
NCT04519645
terminated; "Study stopped after agreed PIP modification, not linked to safety reasons."
recorded 2026-09-01 · last checked 2026-09-04
Q4
Human studies of Erlosamide used Lacosamide 100 mg — over how long?
Human studies of Erlosamide used "Lacosamide 100 mg". ClinicalTrials.gov · 2026-09-01
12 recorded entries; human; capsule; also "Vimpat 50mg; 100mg; 150mg; 200mg", "Lacosamide (200 mg/20 mL)", "Placebo capsule identical in appearance to Lacosamide 100 mg and 200 mg capsules."
Show the evidence
human
NCT01710657
Lacosamide 100 mg
NCT01858870
Vimpat 50mg; 100mg; 150mg; 200mg
NCT02192814
Lacosamide (200 mg/20 mL)
NCT03897348
capsule; Placebo capsule identical in appearance to Lacosamide 100 mg and 200 mg capsules.
NCT03897348
capsule; Lacosamide 100 mg capsule identical in appearance to Placebo and Lacosamide 200 mg capsule
NCT03897348
capsule; Lacosamide 200 mg capsule identical in appearance to Placebo and Lacosamide 100 mg capsules.
6 more recorded rows
humanNCT05598905
Lacosamide 150 mg
humanNCT05598905
capsule; Vimpat 150 mg capsule
humanNCT05626140
Lacosamide 50 MG Oral Tablet [Vimpat]
humanNCT05626140
Vimpat 50 mg
humanNCT05632133
Lacosamide 50 MG Oral Tablet
humanNCT06243692
Lacosamide 50 MG
recorded 2026-09-01 · last checked 2026-09-04
Q5
Erlosamide's half-life is 13 hours — which schedules were studied?
13 hours, the half-life Erlosamide's label states: "The maximum lacosamide plasma concentrations occur approximately 1-to-4-hour post-dose after oral dosing, and elimination half-life is approximately 13 hours." DailyMed label · b9a0ca8c-593c-48e8-b2a7-d30d5f6e6a9b · 2026-08-12
tmax 0.5 to 12 hours; bioavailability 100 %.
Show the evidence
half lifepharmacokinetics
13 hours; The maximum lacosamide plasma concentrations occur approximately 1-to-4-hour post-dose after oral dosing, and elimination half-life is approximately 13 hours.
tmaxpharmacokinetics
0.5 to 12 hours; Compared to lacosamide the major metabolite, O-desmethyl metabolite, has a longer T max (0.5 to 12 hours) and elimination half-life (15 to 23 hours).
bioavailabilitypharmacokinetics
100 %; Lacosamide is completely absorbed after oral administration with negligible first-pass effect with a high absolute bioavailability of approximately 100%.
metabolismpharmacokinetics
Metabolism and Elimination Lacosamide is primarily eliminated from the systemic circulation by renal excretion and biotransformation.
recorded 2026-08-12 · last checked 2026-09-04
Q6
Which 35 trials of Erlosamide posted no result?
Posted no result
35 of 35 completed trials
Registrations
NCT00861068, NCT00861445, NCT01796938, NCT00800215, NCT00238511 and NCT00238524, and 29 more
Completion dates
oldest 2003-01; newest 2024-01-12
Show the evidence
Trial
NCT00861068
2003-01
NCT00861445
2003-02
NCT01796938
2004-11
NCT00800215
2004-11-30
NCT00238511
2005-01
NCT00238524
2005-01
14 further recorded trials
NCT00235469
2005-06
NCT00135109
2005-12
NCT00220415
2006-01
NCT00151879
2006-05
NCT00136019
2006-08
NCT01450111
2009-02
NCT01375387
2011-06
NCT01587339
2011-07
NCT01526083
2012-03
NCT01530386
2012-07
NCT01382017
2012-08
NCT01981447
2012-08
NCT00832884
2012-11
NCT01858870
2012-12
Q7
At the median, Erlosamide's trials enrolled 100 people — anything larger?
Median enrolment
100
Largest enrolment
6498
Registered trials counted
102
Q8
What do 3359 spontaneous reports say about Erlosamide — and not say?
These are reports people sent to a regulator. They do not show the medicine caused the reaction. Nobody counted how many people took the medicine and reported nothing. The same event can be reported more than once, and many reports are incomplete. News coverage, lawsuits and new warnings change how often people report. A count is not a rate and not a risk.
Erlosamide appears in spontaneous reports to regulators. Across the 10 most-reported reaction terms, 3359 reaction mentions were counted: seizure 1019; status epilepticus 476; convulsion 388; epilepsy 355. FAERS via Open Targets · CHEMBL58323 · 2026-06-24
Show the evidence
seizure
1019
status epilepticus
476
convulsion
388
epilepsy
355
generalised tonic-clonic seizure
270
somnolence
257
4 more recorded rows
bradycardia
157
partial seizures
155
multiple-drug resistance
147
drug resistance
135
recorded 2026-06-24 · last checked 2026-09-04
Q9
Which 10 reactions does Erlosamide's label not list?
7.1 Strong CYP3A4 or CYP2C9 Inhibitors Patients with renal or hepatic impairment who are taking strong inhibitors of CYP3A4 and CYP2C9 may have a significant increase in exposure to lacosamide.
pharmacokinetics
The CYP isoforms mainly responsible for the formation of the major metabolite (O-desmethyl) are CYP3A4, CYP2C9, and CYP2C19.
pharmacokinetics
Results from a trial in poor metabolizers (PM) (N=4) and extensive metabolizers (EM) (N=8) of cytochrome P450 (CYP) 2C19 showed that lacosamide plasma concentrations were similar in PMs and EMs, but plasma concentrations and the amount excreted into urine of the O-desmethyl metabolite were about 70% reduced in PMs compared to EMs.
pharmacokinetics
Drug Interactions In Vitro Assessment of Drug Interactions In vitro metabolism studies indicate that lacosamide does not induce the enzyme activity of drug metabolizing cytochrome P450 isoforms CYP1A2, 2B6, 2C9, 2C19 and 3A4.
pharmacokinetics
Lacosamide did not inhibit CYP 1A1, 1A2, 2A6, 2B6, 2C8, 2C9, 2D6, 2E1, 3A4/5 at plasma concentrations observed in clinical studies.
pharmacokinetics
Lacosamide was not a substrate or inhibitor for P-glycoprotein.
2 more recorded rows
Interaction statementpharmacokinetics
Lacosamide is a substrate of CYP3A4, CYP2C9, and CYP2C19.
Interaction statementpharmacokinetics
Patients with renal or hepatic impairment who are taking strong inhibitors of CYP3A4 and CYP2C9 may have increased exposure to lacosamide.
ChEMBL 37 — CC BY-SA 3.0 Unported · ChEMBL ATC CC BY-SA · ClinicalTrials.gov — US Government work · Open Targets 26.06 — CC0 · mixed register set; per-register licences in docs/specs/corpus-20k-sources.md · openFDA / DailyMed — US Government work
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