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Verapamil | CAS No: 52-53-9 | GMP-certified suppliers
A medication that manages angina, hypertension, and supraventricular arrhythmias while supporting ventricular rate control needs in atrial fibrillation for diverse cardiovascular treatment requirements.
Therapeutic categories
ACE Inhibitors and Calcium Channel BlockersAdrenergic alpha-1 Receptor AntagonistsAdrenergic alpha-AntagonistsAdrenergic AntagonistsAminesAntiarrhythmic agents
Generic name
Verapamil
Molecule type
small molecule
CAS number
52-53-9
DrugBank ID
DB00661
Approval status
Approved drug
ATC code
C09BB10
Primary indications
- Verapamil is indicated in the treatment of vasopastic (i
- E
- Prinzmetal's) angina, unstable angina, and chronic stable angina
- It is also indicated to treat hypertension, for the prophylaxis of repetitive paroxysmal supraventricular tachycardia, and in combination with digoxin to control ventricular rate in patients with atrial fibrillation or atrial flutter
Product Snapshot
- Verapamil is a small‑molecule drug supplied mainly as oral solid dosage forms and injectable solutions
- It is used for angina, hypertension, and control of supraventricular arrhythmias
- It is approved in the US and Canada
Clinical Overview
Verapamil (CAS 52-53-9) is a phenylalkylamine, non‑dihydropyridine calcium channel blocker indicated for vasospastic, unstable, and chronic stable angina; hypertension; prophylaxis of paroxysmal supraventricular tachycardia; and ventricular rate control in atrial fibrillation or flutter when used with digoxin. Intravenous formulations are used for acute supraventricular tachyarrhythmias. Off‑label, it is frequently used for cluster headache prophylaxis.
The drug is administered as a racemic mixture. The S‑enantiomer exhibits substantially greater potency at L‑type calcium channels, while the R‑enantiomer contributes less to hemodynamic effects. Both are metabolized predominantly by CYP3A pathways.
Verapamil exerts its pharmacological activity by inhibiting L‑type calcium channels via binding to the Cav1.2 alpha‑1 subunit. Blockade is voltage‑ and frequency‑dependent. Reduced calcium influx relaxes vascular smooth muscle, lowers peripheral resistance, and decreases myocardial oxygen demand, which underlies its antianginal and antihypertensive actions. In cardiac conduction tissue, inhibition of calcium‑dependent depolarization prolongs AV nodal refractoriness and slows conduction, producing rate‑control effects in supraventricular arrhythmias.
Absorption is generally complete but subject to extensive first‑pass metabolism. Immediate‑release products have a short duration requiring multiple daily doses, whereas extended‑release matrices enable once‑daily administration. Verapamil and its metabolites are eliminated by hepatic metabolism with renal excretion of metabolites.
Safety considerations include dose‑dependent bradycardia, hypotension, and negative inotropic effects. Use is contraindicated in severe left ventricular dysfunction or advanced conduction abnormalities without pacing. Clinically relevant interactions arise from its role as both substrate and inhibitor of CYP3A and other CYP isoforms, as well as inhibition of P‑glycoprotein and several transporters.
Common global brand contexts include oral immediate‑release and extended‑release tablets and intravenous formulations for acute arrhythmia management.
For API procurement, suppliers should provide evidence of enantiomeric composition control, validated impurity profiles, and compliance with relevant pharmacopoeial monographs and GMP standards to support formulation and regulatory activities.
The drug is administered as a racemic mixture. The S‑enantiomer exhibits substantially greater potency at L‑type calcium channels, while the R‑enantiomer contributes less to hemodynamic effects. Both are metabolized predominantly by CYP3A pathways.
Verapamil exerts its pharmacological activity by inhibiting L‑type calcium channels via binding to the Cav1.2 alpha‑1 subunit. Blockade is voltage‑ and frequency‑dependent. Reduced calcium influx relaxes vascular smooth muscle, lowers peripheral resistance, and decreases myocardial oxygen demand, which underlies its antianginal and antihypertensive actions. In cardiac conduction tissue, inhibition of calcium‑dependent depolarization prolongs AV nodal refractoriness and slows conduction, producing rate‑control effects in supraventricular arrhythmias.
Absorption is generally complete but subject to extensive first‑pass metabolism. Immediate‑release products have a short duration requiring multiple daily doses, whereas extended‑release matrices enable once‑daily administration. Verapamil and its metabolites are eliminated by hepatic metabolism with renal excretion of metabolites.
Safety considerations include dose‑dependent bradycardia, hypotension, and negative inotropic effects. Use is contraindicated in severe left ventricular dysfunction or advanced conduction abnormalities without pacing. Clinically relevant interactions arise from its role as both substrate and inhibitor of CYP3A and other CYP isoforms, as well as inhibition of P‑glycoprotein and several transporters.
Common global brand contexts include oral immediate‑release and extended‑release tablets and intravenous formulations for acute arrhythmia management.
For API procurement, suppliers should provide evidence of enantiomeric composition control, validated impurity profiles, and compliance with relevant pharmacopoeial monographs and GMP standards to support formulation and regulatory activities.
Identification & chemistry
| Generic name | Verapamil |
|---|---|
| Molecule type | Small molecule |
| CAS | 52-53-9 |
| UNII | CJ0O37KU29 |
| DrugBank ID | DB00661 |
Pharmacology
| Summary | Verapamil primarily blocks L‑type calcium channels in vascular smooth muscle and cardiac tissue, reducing calcium influx that drives contraction and AV nodal conduction. This produces decreased peripheral vascular resistance and moderated cardiac conduction, supporting its use in angina, hypertension, and certain arrhythmias. It also interacts with other calcium channel subtypes and selected potassium and adrenergic targets, which may contribute to effects beyond its core cardiovascular actions. |
|---|---|
| Mechanism of action | Verapamil inhibits L-type calcium channels by binding to a specific area of their alpha-1 subunit,Cav1.2, which is highly expressed on L-type calcium channels in vascular smooth muscle and myocardial tissue where these channels are responsible for the control of peripheral vascular resistance and heart contractility.Calcium influx through these channels allows for the propagation of action potentials necessary for the contraction of muscle tissue and the heart's electrical pacemaker activity. Verapamil binds to these channels in a voltage- and frequency-dependent manner, meaning affinity is increased 1) as vascular smooth muscle membrane potential is reduced, and 2) with excessive depolarizing stimulus. Verapamil's mechanism of action in the treatment of angina and hypertension is likely due to the mechanism described above. Inhibition of calcium influx prevents the contraction of vascular smooth muscle, causing relaxation/dilation of blood vessels throughout the peripheral circulation - this lowers systemic vascular resistance (i.e. afterload) and thus blood pressure. This reduction in vascular resistance also reduces the force against which the heart must push, decreasing myocardial energy consumption and oxygen requirements and thus alleviating angina. Electrical activity through the AV node is responsible for determining heart rate, and this activity is dependent upon calcium influx through L-type calcium channels. By inhibiting these channels and decreasing the influx of calcium, verapamil prolongs the refractory period of the AV node and slows conduction, thereby slowing and controlling the heart rate in patients with arrhythmia. Verapamil's mechanism of action in the treatment of cluster headaches is unclear, but is thought to result from an effect on other calcium channels (e.g. N-, P-, Q-, or T-type). Verapamil is known to interact with other targets, including other calcium channels,potassium channels,and adrenergic receptors. |
| Pharmacodynamics | Verapamil is an L-type calcium channel blocker with antiarrhythmic, antianginal, and antihypertensive activity.Immediate-release verapamil has a relatively short duration of action, requiring dosing 3 to 4 times daily,but extended-release formulations are available that allow for once-daily dosing.As verapamil is a negative inotropic medication (i.e. it decreases the strength of myocardial contraction), it should not be used in patients with severe left ventricular dysfunction or hypertrophic cardiomyopathy as the decrease in contractility caused by verapamil may increase the risk of exacerbating these pre-existing conditions. |
Targets
| Target | Organism | Actions |
|---|---|---|
| Voltage-dependent L-type calcium channel subunit alpha-1C | Humans | inhibitor |
| Voltage-dependent N-type calcium channel subunit alpha-1B | Humans | inhibitor |
| Voltage-dependent P/Q-type calcium channel subunit alpha-1A | Humans | inhibitor |
ADME / PK
| Absorption | More than 90% of orally administered verapamil is absorbed - despite this, bioavailability ranges only from 20% to 30% due to rapid biotransformation following first-pass metabolism in the portal circulation.Absorption kinetic parameters are largely dependent on the specific formulation of verapamil involved. Immediate-release verapamil reaches peak plasma concentrations (i.e. T<sub>max</sub>) between 1-2 hours following administration,whereas sustained-release formulations tend to have a T<sub>max</sub> between 6 - 11 hours. AUC and C<sub>max</sub> values are similarly dependent upon formulation. Chronic administration of immediate-release verapamil every 6 hours resulted in plasma concentrations between 125 and 400 ng/mL.Steady-state AUC<sub>0-24h</sub> and C<sub>max</sub> values for a sustained-release formulation were 1037 ng∙h/ml and 77.8 ng/mL for the R-isomer and 195 ng∙h/ml and 16.8 ng/mL for the S-isomer, respectively. Interestingly, the absorption kinetics of verapamil are highly stereospecific - following oral administration of immediate-release verapamil every 8 hours, the relative systemic availability of the S-enantiomer compared to the R-enantiomer was 13% after a single dose and 18% at steady-state. |
|---|---|
| Half-life | Single-dose studies of immediate-release verapamil have demonstrated an elimination half-life of 2.8 to 7.4 hours, which increases to 4.5 to 12.0 hours following repetitive dosing.The elimination half-life is also prolonged in patients with hepatic insufficiency (14 to 16 hours) and in the elderly (approximately 20 hours).Intravenously administered verapamil has rapid distribution phase half-life of approximately 4 minutes, followed by a terminal elimination phase half-life of 2 to 5 hours. |
| Protein binding | Verapamil is extensively protein-bound in plasma. R-verapamil is 94% bound to serum albumin while S-verapamil is 88% bound. Additionally, R-verapamil is 92% bound to alpha-1 acid glycoprotein and S-verapamil is 86% bound. |
| Metabolism | Verapamil is extensively metabolized by the liver, with up to 80% of an administered dose subject to elimination via pre-systemic metabolism - interestingly, this first-pass metabolism appears to clear the S-enantiomer of verapamil much faster than the R-enantiomer.The remaining parent drug undergoes O-demethylation, N-dealkylation, and N-demethylation to a number of different metabolites via the cytochrome P450 enzyme system.Norverapamil, one of the major circulating metabolites, is the result of verapamil's N-demethylation via CYP2C8, CYP3A4, and CYP3A5,and carries approximately 20% of the cardiovascular activity of its parent drug.The other major pathway involved in verapamil metabolism is N-dealkylation via CYP2C8, CYP3A4, and CYP1A2 to the D-617 metabolite. Both norverapamil and D-617 are further metabolized by other CYP isoenzymes to various secondary metabolites. CYP2D6 and CYP2E1 have also been implicated in the metabolic pathway of verapamil, albeit to a minor extent.Minor pathways of verapamil metabolism involve its O-demethylation to D-703 via CYP2C8, CYP2C9, and CYP2C18, and to D-702 via CYP2C9 and CYP2C18. Several steps in verapamil's metabolic pathway show stereoselective preference for the S-enantiomer of the given substrate, including the generation of the D-620 metabolite by CYP3A4/5 and the D-617 metabolite by CYP2C8. |
| Route of elimination | Approximately 70% of an administered dose is excreted as metabolites in the urine and ≥16% in the feces within 5 days. Approximately 3% - 4% is excreted in the urine as unchanged drug. |
| Volume of distribution | Verapamil has a steady-state volume of distribution of approximately 300L for its R-enantiomer and 500L for its S-enantiomer. |
| Clearance | Systemic clearance following 3 weeks of continuous treatment was approximately 340 mL/min for R-verapamil and 664 mL/min for S-verapamil.Of note, apparent oral clearance appears to vary significantly between single dose and multiple-dose conditions. The apparent oral clearance following single doses of verapamil was approximately 1007 mL/min for R-verapamil and 5481 mL/min for S-verapamil, whereas 3 weeks of continuous treatment resulted in apparent oral clearance values of approximately 651 mL/min for R-verapamil and 2855 mL/min for S-verapamil. |
Formulation & handling
- Oral products require solubility enhancement strategies due to very low aqueous solubility and high lipophilicity, with multiple extended‑release technologies commonly used to modulate absorption.
- IV formulations rely on soluble salt forms and require attention to pH control to maintain solution stability.
- Food interactions (notably grapefruit) can alter exposure, so oral formulations may require labeling or design considerations to mitigate variability.
Regulatory status
| Lifecycle | The API’s key U.S. patents expired in 2009 and 2017, indicating that it is well past initial exclusivity. With products marketed in the United States and Canada, the molecule is in a mature stage of its lifecycle with established generic availability likely. |
|---|
| Markets | Canada, US |
|---|
Supply Chain
| Supply chain summary | Verapamil is supplied by numerous manufacturers and repackagers, indicating a mature market dominated by generic producers rather than a single active originator. Branded and generic products are established in North America, with distribution documented in both the United States and Canada. Listed U.S. patents have expired, consistent with the wide availability of existing generic competition. |
|---|
Safety
| Toxicity | Verapamil's reported oral TDLo is 14.4 mg/kg in women and 3.429 mg/kg in men.The oral LD<sub>50</sub> is 150 mg/kg in rats and 163 mg/kg in mice. As there is no antidote for verapamil overdosage, treatment is largely supportive. Symptoms of overdose are generally consistent with verapamil's adverse effect profile (i.e. hypotension, bradycardia, arrhythmia) but instances of non-cardiogenic pulmonary edema have been observed following ingestion of large overdoses (up to 9 grams).In acute overdosage, consider the use of gastrointestinal decontamination with cathartics and/or bowel irrigation. Patients presenting with significant myocardial depression may require intravenous calcium, atropine, vasopressors, or other inotropes. Consider the formulation responsible for the overdose prior to treatment - sustained-release formulations may result in delayed pharmacodynamic effects, and these patients should be monitored closely for at least 48 hours following ingestion. |
|---|
High Level Warnings:
- Reported human oral TDLo values show sex‑dependent variability (≈14
- 4 mg/kg in women
- ≈3
Verapamil is a type of Calcium Channel Blockers
Calcium channel blockers (CCBs) are a subcategory of pharmaceutical active pharmaceutical ingredients (APIs) widely used in the treatment of various cardiovascular conditions. CCBs work by blocking the influx of calcium ions into smooth muscle cells and cardiac muscle cells, leading to vasodilation and reduced cardiac contractility.
CCBs are commonly prescribed to manage hypertension (high blood pressure), angina (chest pain), and certain arrhythmias (irregular heart rhythms). They are also effective in treating Raynaud's disease and migraine headaches. These medications exert their therapeutic effects by selectively inhibiting L-type calcium channels in the heart and blood vessels.
By blocking calcium channels, CCBs help relax and widen blood vessels, reducing peripheral resistance and improving blood flow. This mechanism of action lowers blood pressure, relieves angina symptoms, and helps prevent certain types of abnormal heart rhythms.
Some well-known CCBs include amlodipine, nifedipine, diltiazem, and verapamil. These medications are available in various formulations, including immediate-release and extended-release tablets, as well as injectable solutions.
It's important to note that CCBs may cause certain side effects, such as dizziness, headache, flushing, and ankle swelling. They may also interact with other medications, so it's crucial to consult a healthcare professional before starting or changing any CCB therapy.
In summary, Calcium channel blockers are a subcategory of cardiovascular medications that inhibit calcium channels, resulting in vasodilation, decreased cardiac contractility, and overall therapeutic effects in conditions such as hypertension, angina, and arrhythmias. Proper medical supervision and individualized treatment plans are essential for optimizing the use of CCBs.
Verapamil (Calcium Channel Blockers), classified under Antihypertensive agents
Antihypertensive agents are a crucial category of pharmaceutical active pharmaceutical ingredients (APIs) used to treat high blood pressure, also known as hypertension. These medications are designed to lower blood pressure and reduce the risk of associated cardiovascular complications.
Antihypertensive agents function by targeting various mechanisms involved in blood pressure regulation. Some common classes of antihypertensive agents include angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), beta-blockers, calcium channel blockers (CCBs), and diuretics.
ACE inhibitors work by inhibiting the enzyme responsible for converting angiotensin I to angiotensin II, a hormone that constricts blood vessels. ARBs, on the other hand, block the receptors to which angiotensin II binds, thereby preventing its vasoconstrictive effects.
Beta-blockers reduce blood pressure by blocking the effects of adrenaline and noradrenaline, which are responsible for increasing heart rate and constricting blood vessels. CCBs inhibit calcium from entering the smooth muscles of blood vessels, resulting in relaxation and vasodilation. Diuretics promote the elimination of excess fluid and sodium from the body, reducing blood volume and thereby lowering blood pressure.
Antihypertensive agents are typically prescribed based on the individual patient's condition and specific needs. They can be used alone or in combination to achieve optimal blood pressure control. It is important to note that antihypertensive agents should be taken regularly as prescribed by a healthcare professional and may require periodic monitoring to ensure their effectiveness and manage any potential side effects.
In summary, antihypertensive agents play a vital role in the management of hypertension by targeting various mechanisms involved in blood pressure regulation. These medications offer significant benefits in reducing the risk of cardiovascular complications associated with high blood pressure.
Verapamil API manufacturers & distributors
Compare qualified Verapamil API suppliers worldwide. We currently have 9 companies offering Verapamil API, with manufacturing taking place in 4 different countries. Use the table below to review supplier type, countries of origin, certifications, product portfolio and GMP audit availability.
| Supplier | Type | Country | Product origin | Certifications | Portfolio |
|---|---|---|---|---|---|
| Abbott Labs | Producer | United States | United States | CEP, CoA, GMP, USDMF | 4 products |
| Assurgen Pharma | Producer | India | India | CoA, WC | 3 products |
| Global Pharma Tek | Distributor | India | India | BSE/TSE, CoA, FDA, GMP, ISO9001, MSDS | 484 products |
| Mylan | Producer | India | India | CoA, USDMF | 201 products |
| Piramal Healthcare | Producer | United Kingdom | India | CoA, GMP, WC | 31 products |
| Piramal Pharma Solutions | Producer | India | Unknown | CEP, CoA, FDA, GMP, USDMF, WC | 44 products |
| Recordati S.p.A. | Producer | Italy | Italy | CEP, CoA, FDA, JDMF, USDMF | 18 products |
| Socosur | Distributor | France | Unknown | CoA | 21 products |
| Tenatra Exports Private L... | Distributor | India | India | BSE/TSE, CoA, FDA, GMP, MSDS | 263 products |
When sending a request, specify which Verapamil API quality you need: for example EP (Ph. Eur.), USP, JP, BP, or another pharmacopoeial standard, as well as the required grade (base, salt, micronised, specific purity, etc.).
Use the list above to find high-quality Verapamil API suppliers. For example, you can select GMP, FDA or ISO certified suppliers. Visit our help page to learn more about sourcing APIs via Pharmaoffer.
Frequently asked questions about Verapamil API
Sourcing
What matters most when sourcing GMP-grade Verapamil?
Key considerations include confirming GMP compliance and ensuring the supplier can provide complete regulatory documentation suitable for U.S. and Canadian requirements. Given the mature generic market, verifying the manufacturer’s quality systems and supply chain traceability is essential. It is also important to assess consistency of batch availability across multiple producers due to the broad sourcing landscape.
Which documents are typically required when sourcing Verapamil API?
Request the core API documentation set: CoA (9 companies), GMP (5 companies), USDMF (4 companies), FDA (4 companies), CEP (3 companies). Confirm versions and validity dates match the destination market to avoid delays in qualification.
Which manufacturers are known to produce Verapamil API?
Known or reported manufacturers for Verapamil: Global Pharma Tek, Tenatra Exports Private Limited. Evaluate their GMP history, scale, and regional coverage before requesting dossiers or allocating demand.
How can I request quotes for Verapamil API from GMP suppliers?
Submit quote requests through the supplier listings with your specs and required documents (specifications, target volume, delivery timeline, and destination). Providing consistent details upfront speeds comparable offers and clarifies technical feasibility.
Is a GMP audit report available for Verapamil manufacturers?
Audit reports may be requested for Verapamil: 3 GMP audit reports available. Confirm the scope and recency of any audit before relying on it for qualification decisions.
How many suppliers offer Verapamil API on Pharmaoffer?
Reported supplier count for Verapamil: 9 verified suppliers. Filter listings by certifications, regions, and delivery options to match your qualification plan.
Which countries are known to manufacture Verapamil API?
Production countries reported for Verapamil: India (5 producers), Italy (1 producer), United States (1 producer). Knowing the manufacturing geography helps anticipate logistics lead times and import compliance needs.
Which certifications do suppliers of Verapamil usually hold?
Common certifications for Verapamil suppliers: CoA (9 companies), GMP (5 companies), USDMF (4 companies), FDA (4 companies), CEP (3 companies). Always verify issuing authorities and expiry dates when reviewing audit packages.
Technical
What is Verapamil (CAS 52-53-9) used for?
Verapamil is used to treat vasospastic, unstable, and chronic stable angina, hypertension, and several supraventricular arrhythmias. It is also used for prophylaxis of paroxysmal supraventricular tachycardia and for ventricular rate control in atrial fibrillation or flutter when given with digoxin. Intravenous formulations are used for acute supraventricular tachyarrhythmias, and it is also employed off‑label for cluster headache prophylaxis.
Which therapeutic class does Verapamil fall into?
Verapamil belongs to the following therapeutic categories: ACE Inhibitors and Calcium Channel Blockers, Adrenergic alpha-1 Receptor Antagonists, Adrenergic alpha-Antagonists, Adrenergic Antagonists, Amines. This positioning helps teams compare alternative APIs, anticipate pharmacology expectations, and align early research priorities.
What conditions is Verapamil mainly prescribed for?
The primary indications for Verapamil: Verapamil is indicated in the treatment of vasopastic (i, E, Prinzmetal's) angina, unstable angina, and chronic stable angina, It is also indicated to treat hypertension, for the prophylaxis of repetitive paroxysmal supraventricular tachycardia, and in combination with digoxin to control ventricular rate in patients with atrial fibrillation or atrial flutter. These use cases frame the target patient populations and help prioritize formulation and safety evaluations.
How does Verapamil work?
Verapamil inhibits L-type calcium channels by binding to a specific area of their alpha-1 subunit,Cav1.2, which is highly expressed on L-type calcium channels in vascular smooth muscle and myocardial tissue where these channels are responsible for the control of peripheral vascular resistance and heart contractility.Calcium influx through these channels allows for the propagation of action potentials necessary for the contraction of muscle tissue and the heart's electrical pacemaker activity. Verapamil binds to these channels in a voltage- and frequency-dependent manner, meaning affinity is increased 1) as vascular smooth muscle membrane potential is reduced, and 2) with excessive depolarizing stimulus.
Verapamil's mechanism of action in the treatment of angina and hypertension is likely due to the mechanism described above. Inhibition of calcium influx prevents the contraction of vascular smooth muscle, causing relaxation/dilation of blood vessels throughout the peripheral circulation - this lowers systemic vascular resistance (i.e. afterload) and thus blood pressure. This reduction in vascular resistance also reduces the force against which the heart must push, decreasing myocardial energy consumption and oxygen requirements and thus alleviating angina.
Electrical activity through the AV node is responsible for determining heart rate, and this activity is dependent upon calcium influx through L-type calcium channels. By inhibiting these channels and decreasing the influx of calcium, Verapamil prolongs the refractory period of the AV node and slows conduction, thereby slowing and controlling the heart rate in patients with arrhythmia.
Verapamil's mechanism of action in the treatment of cluster headaches is unclear, but is thought to result from an effect on other calcium channels (e.g. N-, P-, Q-, or T-type).
Verapamil is known to interact with other targets, including other calcium channels,potassium channels,and adrenergic receptors.
What should someone know about the safety or toxicity profile of Verapamil?
Verapamil’s safety profile is characterized by dose‑dependent bradycardia, hypotension, and negative inotropic effects, which can be clinically significant in patients with impaired ventricular function or conduction disease. Reported human oral TDLo values indicate sex‑dependent variability. The drug is contraindicated in severe left ventricular dysfunction or advanced AV block without pacing. Clinically relevant interactions occur because it is both a CYP3A substrate and inhibitor and also inhibits P‑glycoprotein and other transporters.
What are important formulation and handling considerations for Verapamil as an API?
Formulation of Verapamil requires strategies to address its very low aqueous solubility and high lipophilicity, often through solubility‑enhancing approaches or extended‑release technologies to control absorption and variability. For IV products, use of soluble salt forms and careful pH control is needed to maintain solution stability. Oral formulations should also account for food‑related exposure changes, including interactions such as with grapefruit, which may require appropriate labeling or design considerations.
Is Verapamil a small molecule?
Verapamil is classified as a small molecule. That classification shapes process design, impurity profiling, and analytical control strategies.
Are there special stability concerns for oral Verapamil?
Oral Verapamil has very low aqueous solubility and high lipophilicity, so formulations often require solubility‑enhancing or extended‑release technologies to maintain consistent performance. Extended‑release systems are used to modulate absorption, which is sensitive to formulation design. Food effects, including interactions with grapefruit, can alter exposure and may necessitate labeling or formulation considerations to reduce variability. Stability concerns therefore center on maintaining solubility and controlled release throughout shelf life.
Regulatory
Where is Verapamil approved or in use globally?
Verapamil is reported as approved in the following major regions: Canada, US. Understanding geographic coverage informs regulatory filings, supply planning, and risk assessments before escalating procurement.
What’s the regulatory and patent landscape for Verapamil right now?
Verapamil is an established active ingredient with regulatory approvals in the United States and Canada. The context does not include patent information, so no current patent status can be described.
Pharmaoffer
How does Pharmaoffer’s Smart Sourcing Service help with Verapamil procurement?
Pharmaoffer's Smart Sourcing Service coordinates compliant suppliers, documentation, and competitive quotes for Verapamil. It centralizes outreach, follow-ups, and document validation to shorten procurement timelines.
Is Verapamil included in the PRO Data Insights coverage?
PRO Data Insights coverage for Verapamil: 1343 verified transactions across 334 suppliers and 169 buyers worldwide. Use the dataset to benchmark suppliers and monitor regulatory activity where available.
Where can I access the API market report for Verapamil?
Market report availability for Verapamil: Report Available. The report highlights demand trends, pricing drivers, and supplier landscape insights for procurement planning.
