CLINICAL TRIALS PROFILE FOR QUINIDINE SULFATE

All Clinical Trials for QUINIDINE SULFATE

Trial ID	Title	Status	Sponsor	Phase	Start Date	Summary
NCT00573443 ↗	Safety and Efficacy of AVP-923 in PBA Patients With ALS or MS	Completed	INC Research	Phase 3	2007-12-01	Objectives of the study are to evaluate the safety, tolerability, and efficacy of two different doses of AVP-923 (capsules containing either 30 mg of dextromethorphan hydrobromide and 10 mg of quinidine sulfate [AVP-923-30] or 20 mg of dextromethorphan hydrobromide and 10 mg of quinidine sulfate [AVP-923-20]) when compared to placebo, for the treatment of PBA in a population of patients with amyotrophic lateral sclerosis (ALS) or multiple sclerosis (MS) over a 12-week period. An additional objective is to determine the pharmacokinetic parameters of the two different doses of AVP-923 in a subset of the study population. Pseudobulbar Affect (PBA) is a condition characterized by involuntary, sudden and frequent episodes of laughing and/or crying out of proportion or incongruous to the underlying emotion of happiness or sadness Other terms used to describe this condition include emotional lability, emotionalism, emotional incontinence, emotional discontrol, excessive emotionalism, and pathological laughing and crying. The outbursts can occur spontaneously or in response to provocative stimuli such as questions or events. A body of evidence suggests that PBA can be modulated through pharmacologic intervention. Dextromethorphan (DM) is a low-affinity uncompetitive antagonist of the N-Methyl-D-aspartate (NMDA) receptor, reducing the level of excitatory activity. DM also acts at the phencyclidine-binding site, which is part of the NMDA receptor complex. DM is a sigma receptor agonist, suppressing the release of excitatory neurotransmitters. Quinidine (Q) is a known potent inhibitor of cytochrome P450 2D6 (CYP2D6), that decreases the metabolism of dextromethorphan and helps to achieve sustained and therapeutic levels of this drug.
NCT00573443 ↗	Safety and Efficacy of AVP-923 in PBA Patients With ALS or MS	Completed	Syneos Health	Phase 3	2007-12-01	Objectives of the study are to evaluate the safety, tolerability, and efficacy of two different doses of AVP-923 (capsules containing either 30 mg of dextromethorphan hydrobromide and 10 mg of quinidine sulfate [AVP-923-30] or 20 mg of dextromethorphan hydrobromide and 10 mg of quinidine sulfate [AVP-923-20]) when compared to placebo, for the treatment of PBA in a population of patients with amyotrophic lateral sclerosis (ALS) or multiple sclerosis (MS) over a 12-week period. An additional objective is to determine the pharmacokinetic parameters of the two different doses of AVP-923 in a subset of the study population. Pseudobulbar Affect (PBA) is a condition characterized by involuntary, sudden and frequent episodes of laughing and/or crying out of proportion or incongruous to the underlying emotion of happiness or sadness Other terms used to describe this condition include emotional lability, emotionalism, emotional incontinence, emotional discontrol, excessive emotionalism, and pathological laughing and crying. The outbursts can occur spontaneously or in response to provocative stimuli such as questions or events. A body of evidence suggests that PBA can be modulated through pharmacologic intervention. Dextromethorphan (DM) is a low-affinity uncompetitive antagonist of the N-Methyl-D-aspartate (NMDA) receptor, reducing the level of excitatory activity. DM also acts at the phencyclidine-binding site, which is part of the NMDA receptor complex. DM is a sigma receptor agonist, suppressing the release of excitatory neurotransmitters. Quinidine (Q) is a known potent inhibitor of cytochrome P450 2D6 (CYP2D6), that decreases the metabolism of dextromethorphan and helps to achieve sustained and therapeutic levels of this drug.
NCT00573443 ↗	Safety and Efficacy of AVP-923 in PBA Patients With ALS or MS	Completed	Avanir Pharmaceuticals	Phase 3	2007-12-01	Objectives of the study are to evaluate the safety, tolerability, and efficacy of two different doses of AVP-923 (capsules containing either 30 mg of dextromethorphan hydrobromide and 10 mg of quinidine sulfate [AVP-923-30] or 20 mg of dextromethorphan hydrobromide and 10 mg of quinidine sulfate [AVP-923-20]) when compared to placebo, for the treatment of PBA in a population of patients with amyotrophic lateral sclerosis (ALS) or multiple sclerosis (MS) over a 12-week period. An additional objective is to determine the pharmacokinetic parameters of the two different doses of AVP-923 in a subset of the study population. Pseudobulbar Affect (PBA) is a condition characterized by involuntary, sudden and frequent episodes of laughing and/or crying out of proportion or incongruous to the underlying emotion of happiness or sadness Other terms used to describe this condition include emotional lability, emotionalism, emotional incontinence, emotional discontrol, excessive emotionalism, and pathological laughing and crying. The outbursts can occur spontaneously or in response to provocative stimuli such as questions or events. A body of evidence suggests that PBA can be modulated through pharmacologic intervention. Dextromethorphan (DM) is a low-affinity uncompetitive antagonist of the N-Methyl-D-aspartate (NMDA) receptor, reducing the level of excitatory activity. DM also acts at the phencyclidine-binding site, which is part of the NMDA receptor complex. DM is a sigma receptor agonist, suppressing the release of excitatory neurotransmitters. Quinidine (Q) is a known potent inhibitor of cytochrome P450 2D6 (CYP2D6), that decreases the metabolism of dextromethorphan and helps to achieve sustained and therapeutic levels of this drug.
NCT01873950 ↗	Study of the Electrocardiographic Effects of Ranolazine, Dofetilide, Verapamil, and Quinidine in Healthy Subjects	Completed	Spaulding Clinical Research LLC	Phase 1	2013-05-01	This study seeks to compare 4 known QT prolonging drugs versus placebo to determine their effects on electrophysiological and other clinical parameters. The underlying purpose is to determine if depolarization and repolarization effects caused by drugs with differing ionic channel mechanisms can be distinguished from one another, and to gauge the sensitivity and specificity of novel signal analyses for detection of depolarization and repolarization changes. Secondarily, to evaluate the exposure response relationship and drug induced effects on the heart rate biomarker relationship.
NCT01873950 ↗	Study of the Electrocardiographic Effects of Ranolazine, Dofetilide, Verapamil, and Quinidine in Healthy Subjects	Completed	Food and Drug Administration (FDA)	Phase 1	2013-05-01	This study seeks to compare 4 known QT prolonging drugs versus placebo to determine their effects on electrophysiological and other clinical parameters. The underlying purpose is to determine if depolarization and repolarization effects caused by drugs with differing ionic channel mechanisms can be distinguished from one another, and to gauge the sensitivity and specificity of novel signal analyses for detection of depolarization and repolarization changes. Secondarily, to evaluate the exposure response relationship and drug induced effects on the heart rate biomarker relationship.
NCT02153502 ↗	Efficacy, Safety, and Tolerability Study of AVP-786 as an Adjunctive Therapy in Patients With Major Depressive Disorder With an Inadequate Response to Antidepressant Treatment	Completed	Avanir Pharmaceuticals	Phase 2	2014-07-01	The objectives of this 10-week study are to evaluate the efficacy, safety, and tolerability of AVP 786 as an adjunctive therapy compared with placebo in patients with major depressive disorder (MDD) who have shown an inadequate response to standard antidepressant treatment. A secondary objective of this study is to assess the pharmacokinetics (PK) of AVP-786 and potential correlations with pharmacodynamic effects.

Clinical Trial Conditions for QUINIDINE SULFATE

Condition Name

Condition Name for QUINIDINE SULFATE
Intervention	Trials
Agitation in Patients With Dementia of the Alzheimer's Type	6
Healthy	3
Schizophrenia	2
Healthy Adult Male and Female Volunteers	1

Condition MeSH

Condition MeSH for QUINIDINE SULFATE
Intervention	Trials
Psychomotor Agitation	7
Dementia	6
Alzheimer Disease	6
Motor Neuron Disease	2

Clinical Trial Locations for QUINIDINE SULFATE

Trials by Country

Trials by Country for QUINIDINE SULFATE
Location	Trials
United States	235
Brazil	6
Canada	6
Hungary	4
Poland	4

Trials by US State

Trials by US State for QUINIDINE SULFATE
Location	Trials
Florida	14
Ohio	11
New York	11
Georgia	11
California	11

Clinical Trial Progress for QUINIDINE SULFATE

Clinical Trial Phase

Clinical Trial Phase for QUINIDINE SULFATE
Clinical Trial Phase	Trials
Phase 4	1
Phase 3	7
Phase 2/Phase 3	1

Clinical Trial Status

Clinical Trial Status for QUINIDINE SULFATE
Clinical Trial Phase	Trials
Completed	11
Recruiting	6
Terminated	3

Clinical Trial Sponsors for QUINIDINE SULFATE

Sponsor Name

Sponsor Name for QUINIDINE SULFATE
Sponsor	Trials
Avanir Pharmaceuticals	17
Boehringer Ingelheim	2
Food and Drug Administration (FDA)	1

Sponsor Type

Sponsor Type for QUINIDINE SULFATE
Sponsor	Trials
Industry	19
Other	6
U.S. Fed	1

Last updated: July 27, 2026

Quinidine Sulfate clinical trials update, market analysis, and exclusivity/patent-driven generic biosimilar risk

Quinidine sulfate is an established, off-patent antiarrhythmic (quinidine class). Current commercially meaningful market activity in the US is driven by supply continuity, substitution to other antiarrhythmics, and generic availability rather than new entrants secured by exclusivity. Under the US regulatory framework, quinidine sulfate’s entry pathway is generally a generic (ANDA) rather than an innovator-style exclusivity event, because the drug’s active ingredient and long-standing formulations are not tied to a current brand-originated Orange Book exclusivity regime in the same way as newer small molecules.

What is quinidine sulfate’s current FDA regulatory status and Orange Book listing picture?

Is quinidine sulfate listed in the FDA Orange Book, and what does that imply

For a marketed prescription drug with active ingredient “quinidine sulfate,” FDA’s Orange Book typically lists approved application(s) and patent/spinout entries tied to drug product and, in some cases, formulation or method-of-use patents when still active. For an old, widely used API, the practical market impact is usually that patent and exclusivity protections have expired or are limited to legacy product-specific listings. That leads to:

• Multiple approved generic equivalents.
• No meaningful “new formulation” exclusivity that blocks standard generic manufacture.
• Clinical trials that are primarily reformulation, bioequivalence, or comparative effectiveness rather than NDA-style de novo innovation.

Which regulatory pathway dominates

For most quinidine sulfate products, the dominant expectation is:

• Generic entry via ANDA (bioequivalence to a listed reference listed drug).
• Clinical development mainly supports bioequivalence (BE) rather than new clinical endpoints.

What clinical trials are actually happening for quinidine sulfate right now?

Why “clinical trials” for quinidine sulfate are usually BE or comparative studies

Quinidine sulfate is used for specific arrhythmia indications, and its risk profile (notably proarrhythmia/QT effects) shapes trial design. In practice, most “current” trial activity for older antiarrhythmics tends to be:

• Small comparative studies against alternative antiarrhythmics.
• Pharmacokinetic (PK) and pharmacokinetic-pharmacodynamic (PK-PD) studies to support BE.
• Limited investigator-initiated work on dosing, monitoring, or special populations (for example, renal impairment).

How to interpret a “clinical trials update” for an off-patent drug

A business-relevant clinical update for quinidine sulfate is not “pipeline optionality” in the NDA sense. It is instead:

• Trial activity that signals manufacturing risk, supply continuity, or regulatory maintenance needs for specific dosage forms (IR vs ER).
• Trial activity that indicates prescriber practice patterns and switching risk from other antiarrhythmics.

When does quinidine sulfate lose exclusivity and what are the likely generic entry risks?

What “exclusivity” usually means for an older small molecule

For quinidine sulfate as an API, the biggest impact is expiration of:

• Composition-of-matter patents (historically long expired).
• Formulation/process patents (typically product-specific and also usually expired).
• Any residual exclusivity tied to a specific NDA/ANDA reference.

The practical consequence is that generic entry risk is low from a patent-blocking standpoint and higher from:

• Product availability and manufacturing capability.
• Supply chain disruptions.
• Label constraints and cross-reference to a current reference listed drug.

Paragraph IV vs non-Paragraph IV exposure

For an off-patent API with mature generic competition, Paragraph IV litigation is usually not a central driver. If ANDA filers still find patent listings in the Orange Book for a particular product, a Paragraph IV challenge is possible, but the historical pattern for quinidine sulfate is that protections are unlikely to block routine generic market expansion for long.

What patents protect quinidine sulfate, and how strong is the patent estate?

Patent estate strength: typically low for API-level protection

Quinidine sulfate is a classic antiarrhythmic. For business planning, the key is that patent protection is usually:

• Expired at the API level (quinidine base and quinidine sulfate composition history is long).
• Potentially limited to legacy product formulations, specific salts, specific dosage forms, or tightly scoped methods-of-use that are also likely expired or not enforceable.

What to check for enforcement risk

When evaluating legal risk for competitive entry in quinidine sulfate, the relevant buckets are:

• Orange Book patent listings for the specific dosage form (tablets/capsules) and manufacturer reference listed drug (RLD).
• Any continuing enforcement around formulation or process that would affect BE materials, dissolution profile, or manufacturing controls.
• Method-of-use patents (less common in classic antiarrhythmics after broad clinical history).

Which companies market quinidine sulfate and how does competitive positioning affect pricing?

Competition is primarily generic

Quinidine sulfate market pricing is typically driven by:

• Number of ANDA competitors for the same dosage strength and dosage form.
• Price competition dynamics and pharmacy reimbursement.
• Supply constraints and manufacturing attrition for older generic SKUs.

What matters commercially

For an off-patent drug, commercially meaningful differentiators are:

• Product availability and fill rate.
• Submission stability (continued approval, quality).
• Label tolerability and prescriber trust (especially given the narrow therapeutic window of many antiarrhythmics).

How does quinidine sulfate compare with alternative antiarrhythmics in market share and clinical practice?

Competitive substitution risk

Quinidine sulfate is one antiarrhythmic among a broader class that includes:

• Class Ic: flecainide, propafenone.
• Class III: amiodarone, sotalol, dofetilide, dronedarone.
• Others depending on rhythm scenario.

Clinical practice substitution is influenced by:

• Safety monitoring burden (QT, torsades risk).
• Need for ECG and electrolyte management.
• Indication fit and guideline preference.

Implications for projections

Market projections for quinidine sulfate tend to track:

• Share drift toward newer antiarrhythmics.
• Periodic upticks when other options face shortages or access issues.
• Stable baseline demand due to niche guideline use and historical clinician familiarity.

What formulations of quinidine sulfate are marketed, and which product risks can disrupt supply?

Dosage form and dissolution profile matter for generics

For quinidine sulfate, generic approval and substitution depend heavily on BE. For market planning, product risk is often:

• Manufacturing variability that impacts dissolution rate.
• Stability constraints impacting shelf life.
• Filling/dosage-form continuity risk (especially for low-volume strengths).

Commercial risk categories

• Quality events: recalls, warning letters, sterility/cleaning validation issues for related manufacturing lines.
• Capacity risk: aging manufacturing infrastructure for older generics.
• Regulatory maintenance: line changes that trigger supplements and delays.

What does a near-term market projection look like for quinidine sulfate?

Baseline projection logic

Because quinidine sulfate is mature and genericized, projections typically follow:

• Low growth in unit demand.
• Margin pressure from price competition.
• Volatility from supply disruptions.
• Offset from periodic renewed use patterns driven by payer coverage and formulary placement.

Expected direction under current market structure

In the absence of a current, innovation-led exclusivity wave, the most likely near-term pattern is:

• Stable-to-slightly declining volumes due to substitution by other antiarrhythmics and evolving guideline preference.
• Stable generics pricing near cost plus regulated competitive pricing, with episodic spikes during shortages.
• Risk skew to supply rather than patent-driven block.

What clinical endpoints and monitoring requirements shape quinidine sulfate trials?

Common endpoints and safety monitoring

Trials involving quinidine sulfate typically monitor:

• Rhythm control outcomes (conversion, maintenance, recurrence).
• Safety: QT prolongation, proarrhythmic events, torsades risk signals.
• PK/PD alignment for dosing strategies.

Why that matters for any new trial

Safety monitoring intensity limits trial size and timeline. That keeps most “new” activity in the realm of:

• Pharmacology studies
• Comparative effectiveness pilots
• BE and product performance work

Key Takeaways

• Quinidine sulfate’s market and development profile is generic-led and supply-led, not patent-exclusivity-led.
• Clinical trial activity is more likely BE/PK/comparative than NDA-style pipeline expansion.
• Generic entry risks are mainly regulatory and manufacturing-driven, not Paragraph IV-style blocking by active patents.
• Near-term market projections point to stable demand with price pressure and supply-driven volatility, rather than growth from innovation.

FAQs

1. Do quinidine sulfate generics require therapeutic drug monitoring or special PK considerations during substitution?
2. How do QT prolongation and torsades risk requirements affect trial design for quinidine sulfate?
3. What manufacturing or dissolution-profile factors most commonly delay generic approvals for older oral antiarrhythmics like quinidine sulfate?
4. Are there recent shortages or discontinuations that can temporarily lift quinidine sulfate pricing in the US?
5. Which alternative antiarrhythmics most often substitute for quinidine sulfate in rhythm management, and what drives prescriber switching?

References

No sources were provided in the prompt, and none were cited in the response.