CLINICAL TRIALS PROFILE FOR EXTENDED PHENYTOIN SODIUM

All Clinical Trials for EXTENDED PHENYTOIN SODIUM

Trial ID	Title	Status	Sponsor	Phase	Start Date	Summary
NCT00004817 ↗	Phase III Double Blind Trial of Valproate Sodium for Prophylaxis of Post Traumatic Seizures	Completed	Harborview Injury Prevention and Research Center	Phase 3	1991-02-01	OBJECTIVES: I. Determine whether treating head injured patients with valproate sodium will reduce the risk of developing seizures as a result of the head injury. II. Determine the safety of valproate, the appropriate dose, and the effect valproate may have on the recovery of the brain's ability to compute numbers, solve problems, remember information, and control the movement of limbs after head injury.
NCT00004817 ↗	Phase III Double Blind Trial of Valproate Sodium for Prophylaxis of Post Traumatic Seizures	Completed	National Institute of Neurological Disorders and Stroke (NINDS)	Phase 3	1991-02-01	OBJECTIVES: I. Determine whether treating head injured patients with valproate sodium will reduce the risk of developing seizures as a result of the head injury. II. Determine the safety of valproate, the appropriate dose, and the effect valproate may have on the recovery of the brain's ability to compute numbers, solve problems, remember information, and control the movement of limbs after head injury.
NCT00140179 ↗	Valnoctamide in Mania	Completed	Stanley Medical Research Institute	Phase 3	2004-09-01	Valproic acid is a leading mood stabilizer for the treatment of bipolar disorder. Its well-known teratogenicity limits its use in young women of childbearing age. According to toxicologic studies the teratogenicity of valproate stems from its free carboxylic group. Valnoctamide is an isomer and an analog of valpromide. Unlike valpromide, valnoctamide does not undergo a biotransformation to the corresponding free acid. It is also likely or at least possible that valnoctamide is anti-bipolar. In mice valnoctamide has been shown to be distinctly less teratogenic than valproate. An injection at day 8 of gestation produced only 1% exencephaly (as compared to 0-1% in control mice and 53% in valproate treated mice). The investigators are performing a double-blind controlled trial of valnoctamide as an anti-bipolar drug. If shown to be anti-bipolar, valnoctamide could be an important valproate substitute for young women with bipolar disorder who are at risk of pregnancy. Patients newly admitted to the Beersheva Mental Health Center may participate if they meet Diagnostic and Statistical Manual of Mental Disorders - 4th edition (DSM-IV) criteria for mania or schizoaffective disorder, manic type. Patients admitted to the study are treated with risperidone at doses of the physicians' discretion beginning with 2 mg daily on days 1 and 2. Valnoctamide or placebo is begun at doses of 600 mg per day (200 mg three times daily) and increased to 1200 mg (400 mg three times daily) after four days. Weekly ratings by a psychiatrist blind to the study drug are conducted using the Brief Psychiatric Rating Scale (BPRS), the Young Mania Rating Scale (YMS), and the Clinical Global Impression (CGI). Weekly blood is drawn for drug levels of valnoctamide to be measured by gas chromatography. Each patient receives valnoctamide or placebo for 5 weeks. Low teratogenic mood stabilizers are a high priority for current research.
NCT00140179 ↗	Valnoctamide in Mania	Completed	Beersheva Mental Health Center	Phase 3	2004-09-01	Valproic acid is a leading mood stabilizer for the treatment of bipolar disorder. Its well-known teratogenicity limits its use in young women of childbearing age. According to toxicologic studies the teratogenicity of valproate stems from its free carboxylic group. Valnoctamide is an isomer and an analog of valpromide. Unlike valpromide, valnoctamide does not undergo a biotransformation to the corresponding free acid. It is also likely or at least possible that valnoctamide is anti-bipolar. In mice valnoctamide has been shown to be distinctly less teratogenic than valproate. An injection at day 8 of gestation produced only 1% exencephaly (as compared to 0-1% in control mice and 53% in valproate treated mice). The investigators are performing a double-blind controlled trial of valnoctamide as an anti-bipolar drug. If shown to be anti-bipolar, valnoctamide could be an important valproate substitute for young women with bipolar disorder who are at risk of pregnancy. Patients newly admitted to the Beersheva Mental Health Center may participate if they meet Diagnostic and Statistical Manual of Mental Disorders - 4th edition (DSM-IV) criteria for mania or schizoaffective disorder, manic type. Patients admitted to the study are treated with risperidone at doses of the physicians' discretion beginning with 2 mg daily on days 1 and 2. Valnoctamide or placebo is begun at doses of 600 mg per day (200 mg three times daily) and increased to 1200 mg (400 mg three times daily) after four days. Weekly ratings by a psychiatrist blind to the study drug are conducted using the Brief Psychiatric Rating Scale (BPRS), the Young Mania Rating Scale (YMS), and the Clinical Global Impression (CGI). Weekly blood is drawn for drug levels of valnoctamide to be measured by gas chromatography. Each patient receives valnoctamide or placebo for 5 weeks. Low teratogenic mood stabilizers are a high priority for current research.
NCT00257855 ↗	A Randomised Controlled Trial of Neuroprotection With Lamotrigine in Secondary Progressive Multiple Sclerosis	Completed	University College London Hospitals	Phase 2	2005-11-01	A present there is no safe treatment for reducing rate at which disability worsens in people with secondary progressive multiple sclerosis. Recent research has suggested the possibility that drugs that act by blocking the entry of sodium into nerve cells can protect nerve fibres in the brain and spinal cord. In this trial, the investigators will test whether one such drug, called lamotrigine, can prevent damage to nerve fibres and reduce the rate at which MS worsens. The period of treatment in the trial will run for 2 years.
NCT00511745 ↗	Safety of Rabeprazole in Patients Under Multiple Treatments	Terminated	Janssen-Cilag, S.A.		1969-12-31	The purpose of this study is to evaluate the safety of rabeprazole 20mg/day in polymedicated patients and to examine the necessity of adjusted dosage in both therapies (rabeprazole and concomitant drug). Proton pump inhibitors (PPI) act in the final step of the gastric secretion. PPI's block ATP-ase H+/K+ in gastric parietals cells. It has been described that inhibition of acid secretion has produced the recovery of the gastroesophageal pathology in a high percentage of the patients resistant to conventional drugs. In this context, the objective of the study is to evaluate the safety of rabeprazole as a concomitant treatment and examine the clinical practice the interaction with drugs whose absorption has gastric pH dependence.
NCT00647621 ↗	Steady-State Study of Extended Phenytoin Sodium Capsules 100 mg and Dilantin® Kapseals® 100 mg	Completed	Mylan Pharmaceuticals	Phase 1	2005-10-01	The objective of this study was to investigate the steady-state bioequivalence of Mylan's extended phenytoin sodium capsules, 100mg (3x100mg), to Pfizer's Dilantin® Kapseals®, 100mg (3x100mg), under both fasting and fed conditions.

Clinical Trial Conditions for EXTENDED PHENYTOIN SODIUM

Condition Name

Condition Name for EXTENDED PHENYTOIN SODIUM
Intervention	Trials
Optic Neuritis	2
Healthy	2
Cerebrovascular Event	1
Hemorrhagic Stroke	1

Condition MeSH

Condition MeSH for EXTENDED PHENYTOIN SODIUM
Intervention	Trials
Sclerosis	2
Optic Neuritis	2
Seizures	2
Neoplasm Metastasis	2

Clinical Trial Locations for EXTENDED PHENYTOIN SODIUM

Trials by Country

Trials by Country for EXTENDED PHENYTOIN SODIUM
Location	Trials
United States	4
United Kingdom	2
China	2
Uganda	1
Iran, Islamic Republic of	1

Trials by US State

Trials by US State for EXTENDED PHENYTOIN SODIUM
Location	Trials
New York	1
Georgia	1
California	1
North Dakota	1

Clinical Trial Progress for EXTENDED PHENYTOIN SODIUM

Clinical Trial Phase

Clinical Trial Phase for EXTENDED PHENYTOIN SODIUM
Clinical Trial Phase	Trials
PHASE4	2
Phase 4	3
Phase 3	4

Clinical Trial Status

Clinical Trial Status for EXTENDED PHENYTOIN SODIUM
Clinical Trial Phase	Trials
Completed	12
Unknown status	3
NOT_YET_RECRUITING	2

Clinical Trial Sponsors for EXTENDED PHENYTOIN SODIUM

Sponsor Name

Sponsor Name for EXTENDED PHENYTOIN SODIUM
Sponsor	Trials
West China Hospital	1
Beersheva Mental Health Center	1
Tanta University	1

Sponsor Type

Sponsor Type for EXTENDED PHENYTOIN SODIUM
Sponsor	Trials
Other	60
Industry	5
OTHER_GOV	2

Extended Phenytoin Sodium clinical trials update, market analysis, and 2026–2036 projection

Last updated: July 28, 2026

Extended phenytoin sodium (extended-release phenytoin sodium; generic and branded versions) remains an entrenched antiepileptic therapy with limited late-stage clinical “value inflection.” Publicly visible clinical-trial activity is dominated by bioequivalence and formulation-related studies, not brand-new therapeutic-efficacy programs. Market growth is largely driven by baseline epilepsy incidence, aging demographics, and substitution dynamics across immediate-release versus extended-release offerings, with pricing pressure from generics and payor formulary controls.

This page compiles (1) the current clinical-trial posture visible in public registries, (2) commercial and adoption drivers, and (3) a structured forecast framework for 2026–2036 based on patent/exclusivity realities for older small-molecule antiepileptics.

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What clinical trials exist for extended phenytoin sodium in 2024–2026?

Answer: Trial activity for extended phenytoin sodium in the 2024–2026 window is primarily bioequivalence, pharmacokinetics (PK), or formulation comparability studies rather than new mechanism-of-action or seizure-endpoint programs.

Where do trials typically show up?

For extended-release phenytoin sodium products, most public entries fall into these buckets:

• Bioequivalence and PK studies comparing one extended-release product versus a reference listed drug (RLD).
• Switching studies assessing steady-state concentrations and tolerability after transitioning from immediate-release phenytoin formulations.
• Safety monitoring studies focusing on adverse event profiles tied to phenytoin exposure (notably neurologic adverse events associated with supratherapeutic levels).

What endpoints are most common?

• Plasma phenytoin exposure metrics (Cmax, Tmax, AUC) and steady-state attainment.
• Tolerability and clinically observed adverse events linked to phenytoin kinetics.
• (In some studies) adherence or seizure diary outcomes, but these are not the dominant public trial design for extended-release phenytoin sodium.

How does this affect competitive strategy?

Because most trials target regulatory demonstration of equivalence rather than novel clinical outcomes, the competitive “fork” is less about clinical differentiation and more about:

• Manufacturing control of release characteristics,
• Bioequivalence success,
• Labeling consistency with therapeutic drug monitoring expectations,
• Brand-specific payer contracting and substitution rules.

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Are there late-stage efficacy trials for extended phenytoin sodium?

Answer: No broad, publicly visible late-stage (Phase 2/3) seizure-efficacy development programs are driving the competitive landscape for extended phenytoin sodium in the current period; activity is mostly regulatory and formulation oriented.

What would “late-stage efficacy” imply?

A true efficacy-driven program would show:

• Seizure frequency responder or time-to-first-seizure endpoints,
• Randomized comparator designs with meaningful control arms,
• Regulatory submissions for new indications or expanded populations.

The extended phenytoin sodium space does not show that pattern in public sources in the way newer antiepileptics do.

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What market dynamics shape demand for extended phenytoin sodium?

Answer: Demand tracks the chronic epilepsy population, with product choice influenced by dosing convenience, prescriber preference for steady exposure, and pharmacy-level substitution economics. Generic substitution and price compression are the dominant commercial forces.

Key demand drivers

• Chronicity: Epilepsy treatment is long-duration, supporting baseline volume.
• Therapeutic drug monitoring reality: Phenytoin has a narrow therapeutic index, so prescribers often emphasize consistent formulation and dosing intervals.
• Dosing convenience: Extended-release regimens reduce daily dosing frequency versus some immediate-release schedules, which can support adherence and continuity of therapy.
• Geriatrics: Older adults often have complex medication regimens; extended-release can reduce dosing burden.

Key supply and pricing drivers

• Generic competition: The extended phenytoin sodium market is largely generic-based.
• Formulary controls: Payors prefer lower-cost equivalents, and pharmacy substitution policies affect market share by strength and NDC-level contract structures.
• Compliance with bioequivalence: Manufacturers compete on successful regulatory demonstration rather than on new clinical performance.

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How many competitors sell extended phenytoin sodium, and how fragmented is the market?

Answer: The market is highly fragmented across multiple generic manufacturers and strengths, with competition occurring at the NDC and contract level rather than the single “brand” level.

Competitive map characteristics

• Many entrants typically participate because phenytoin is off-patent in practice for most major jurisdictions and eras.
• Product differentiation is minimal from a clinical-efficacy standpoint; differences are largely release kinetics consistency, excipient selection, and manufacturing robustness.

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What is the revenue outlook for extended phenytoin sodium through 2036?

Answer: Revenue is projected to be stable-to-slow growing in volume terms but flat-to-declining in value terms due to generic price compression, offset partially by aging-driven epilepsy prevalence growth and intermittent switching from immediate-release to extended-release.

Forecast framing (value vs volume)

A practical projection approach for older generics distinguishes:

• Volume: grows with incidence and population aging.
• Value: constrained by tendering, rebate pressure, and generic price erosion.
• Mix: extended-release mix can increase if payors and prescribers move patients from immediate-release due to tolerability or adherence considerations.

Structured forecast components (2016–2036 logic applied to 2026–2036)

• Baseline epilepsy prevalence growth in aging cohorts
• Penetration of extended-release variants relative to immediate-release
• Ongoing generic competition and pricing pressure
• Substitution and reimbursement policies

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When does extended phenytoin sodium lose exclusivity?

Answer: Extended phenytoin sodium is not expected to have meaningful ongoing exclusivity in the standard sense for the active substance class; most market access is driven by generic availability, not by branded patent lifecycles. Any remaining exclusivity is typically product-specific (formulation/ANDA-specific) and expires on an NDC-by-NDC basis.

What “exclusivity” means in this space

• “Orange Book exclusivity” is usually absent or already expired for core phenytoin dosage forms.
• Remaining barriers are typically manufacturing, labeling, and any newer secondary patents that may affect specific formulations, strengths, or controlled-release characteristics.

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What is the Orange Book status of extended phenytoin sodium products?

Answer: Orange Book status is product-specific; for extended-release phenytoin sodium, listings generally reflect expired or near-expired patent estates for the active ingredient class, with remaining protected periods typically tied to a specific dosage form, strength, or formulation.

Practical implication for entry timing

Generic entry is usually limited by:

• Patents on a specific extended-release formulation,
• Use of specific manufacturing processes,
• Any unexpired regulatory exclusivities applicable at the product level.

Without naming a specific NDA/BLA or NDC reference product, a complete Orange Book mapping cannot be produced for this topic at the NDC precision required for litigation-quality analysis.

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How strong is the patent estate for extended phenytoin sodium?

Answer: The patent estate for extended-release phenytoin sodium is generally weak in the sense that the core active ingredient is mature and multiple generic entrants have established shelf competition.

Where patents can still matter

Patent relevance tends to be limited to:

• Secondary formulation/process claims for particular extended-release designs,
• Specific manufacturing method controls,
• Narrow method-of-use claims if any exist for labeling expansion (less common for legacy phenytoin).

For business planning, the key operational point is that most entrants can file ANDAs and focus on bioequivalence and product consistency.

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What generic entry risks exist for extended phenytoin sodium?

Answer: The entry risks are predominantly regulatory and operational, not blockbuster-style IP risk.

Primary risks

• Bioequivalence risk: failing PK similarity at the required statistical thresholds.
• Manufacturing reproducibility risk: altered release characteristics during scale-up or process changes.
• Label consistency risk: mismatches to reference labeling, especially around therapeutic drug monitoring expectations.

Less common risks

• Patent risk: applicable only if a specific manufacturer’s extended-release formulation still has enforceable patents.
• Litigation-driven delays: possible but not a defining feature of the broader extended phenytoin sodium market given the mature asset base.

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How do extended-release and immediate-release phenytoin sodium compete?

Answer: Extended-release competes by dosing convenience and perceived steadier exposure. Immediate-release often competes on historical familiarity and lower-cost availability where immediate-release generics have tighter pricing.

Switching drivers

• Prescriber preference for fewer daily doses.
• Patient adherence and caregiver-administered dosing stability.
• Pharmacy formulary rules favoring one release form by contract.

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What biosimilar risk applies to extended phenytoin sodium?

Answer: None. Phenytoin is a small molecule; biosimilar frameworks do not apply.

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Which companies are positioned to win extended phenytoin sodium market share?

Answer: The likely winners are low-cost suppliers with high bioequivalence success rates, strong manufacturing quality systems, and advantageous contract position with major distributors and pharmacy benefit managers (PBMs). Brand owners and niche manufacturers tend to be less relevant than volume-share efficiency in a generic-dominant market.

Winning attributes

• Competitive unit economics at NDC level
• Reliable supply and low rejection rates
• Fast ANDA response capability and lifecycle management for multiple strengths
• Contracting strength with payors and pharmacy chains

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Clinical and regulatory constraints that shape product success

Answer: Phenytoin’s pharmacokinetic properties and narrow therapeutic window shape both clinical oversight and regulatory labeling, influencing how new extended-release products are adopted.

What matters clinically

• Therapeutic drug monitoring during initiation, titration, and formulation switches
• Adverse event surveillance tied to exposure variability
• Consistency of release behavior over time

What matters for regulators

• Robust bioequivalence demonstration under fed and/or fasting conditions as required
• Dissolution behavior control and in-process validation
• Strength-specific equivalence evidence, because release kinetics can differ by dose level even within the same ER platform

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2026–2036 projection: baseline scenario with sensitivity bands

Answer: The market is projected to grow modestly in units with flat-to-declining pricing, resulting in low single-digit compound annual growth in revenue at best under a “continued generic erosion” scenario. Extended-release mix could add uplift but is unlikely to reverse value erosion.

Projection table (directional, business-planning format)

Period	Expected unit trend	Expected price/unit trend	Net revenue outlook	Key drivers
2026–2028	Low single-digit growth	Flat to declining	Near-flat to low single-digit growth	Generic competition, age-driven prevalence
2029–2031	Low single-digit growth	Continuing decline or stabilization	Low single-digit growth	Mix shifts ER vs IR, contract dynamics
2032–2036	Low single-digit growth	Gradual decline or stabilized low price	Low single-digit growth or flat	Limited differentiation, stable demand base

Main sensitivities

• Extended-release share shift: if payors push ER for adherence, units can rise faster than average.
• PBM rebate pressure: can reduce revenue faster than volume increases.
• Supply disruptions or quality recalls: can temporarily lift pricing for remaining SKUs but create volatility.

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Key takeaways

• Extended phenytoin sodium clinical activity in 2024–2026 is predominantly bioequivalence and formulation comparability, not new efficacy development.
• The market is mature and generic-driven, with competition focused on regulatory success, manufacturing reproducibility, and contract placement.
• Forecast 2026–2036: modest unit growth from baseline epilepsy prevalence and aging demographics, offset by persistent price compression; revenue outlook is low-growth at best.
• IP-driven exclusivity is not a primary commercial variable for the active substance class; product-specific secondary barriers, if any, are typically narrow and NDC-specific.

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FAQs

What is the typical regulatory pathway for extended phenytoin sodium generics?

Most products use an ANDA bioequivalence pathway tied to an FDA reference product, supported by PK and dissolution similarity.

Do extended phenytoin sodium products require therapeutic drug monitoring emphasis on the label?

Yes. Phenytoin’s clinical management generally includes therapeutic drug monitoring expectations during initiation, titration, and formulation changes.

Is there a controlled-release patent landscape for extended phenytoin sodium that blocks generic entry?

Any blocking is typically formulation- or process-specific and depends on the exact reference product and strength; the broader active ingredient is long matured.

How does patient switching from immediate-release to extended-release affect seizure control risk?

Switching requires careful monitoring of plasma levels and adverse effects because phenytoin exposure can vary with formulation and release characteristics.

What endpoints do bioequivalence studies for extended-release phenytoin sodium typically use?

Cmax, Tmax, and AUC for phenytoin under protocol-defined conditions, with safety monitoring for tolerability.

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References

1. FDA. Orange Book: Approved Drug Products with Therapeutic Equivalence Evaluations. U.S. Food and Drug Administration. (Accessed via FDA Orange Book).
2. ClinicalTrials.gov. Search results for “phenytoin sodium extended-release” and related terms. U.S. National Library of Medicine. (Accessed via ClinicalTrials.gov).