CLINICAL TRIALS PROFILE FOR MIOCHOL

All Clinical Trials for MIOCHOL

Trial ID	Title	Status	Sponsor	Phase	Start Date	Summary
NCT01137656 ↗	Storage Lesion in Banked Blood Due to Disruption of Nitric Oxide (NO) Homeostasis	Completed	National Heart, Lung, and Blood Institute (NHLBI)	Phase 1	2010-04-01	The purpose of this study is to explore the impact of aged blood on endothelial function by measuring forearm blood flow during intra-arterial acetylcholine infusion in normal healthy human volunteers after infusion of autologous blood stored for 5-10 days or 35-42 days. Our hypothesis is that 1) the vasodilatory response to the infusion of acetylcholine will be reduced in the 35-42 day group compared with the 5-10 day group, because of scavenging of the NO released from the endothelium by the hemolytic process in the aged blood, 2) that the infusion of aged stored blood will produce vasoconstriction, measured by reduced forearm blood flow during infusion of the 35-42 day compared with the 5-10 day old blood, and that 3) there will be increases in venous levels of cell free plasma hemoglobin, red cell microparticles, red cell membrane damage, arginase levels and activity, decreased arginine levels, markers of oxidative stress (carbamylated proteins and nitrated tyrosine residues), and increases in plasma in vitro NO consumption during the infusion of 35-42 day old compared to 5-10 day old blood.
NCT01137656 ↗	Storage Lesion in Banked Blood Due to Disruption of Nitric Oxide (NO) Homeostasis	Completed	Mark Gladwin	Phase 1	2010-04-01	The purpose of this study is to explore the impact of aged blood on endothelial function by measuring forearm blood flow during intra-arterial acetylcholine infusion in normal healthy human volunteers after infusion of autologous blood stored for 5-10 days or 35-42 days. Our hypothesis is that 1) the vasodilatory response to the infusion of acetylcholine will be reduced in the 35-42 day group compared with the 5-10 day group, because of scavenging of the NO released from the endothelium by the hemolytic process in the aged blood, 2) that the infusion of aged stored blood will produce vasoconstriction, measured by reduced forearm blood flow during infusion of the 35-42 day compared with the 5-10 day old blood, and that 3) there will be increases in venous levels of cell free plasma hemoglobin, red cell microparticles, red cell membrane damage, arginase levels and activity, decreased arginine levels, markers of oxidative stress (carbamylated proteins and nitrated tyrosine residues), and increases in plasma in vitro NO consumption during the infusion of 35-42 day old compared to 5-10 day old blood.
NCT01848301 ↗	Endothelial Injury and Development of Coronary Intimal Thickening After Heart Transplantation	Terminated	Gladwin, Mark, MD	Phase 1	2012-09-01	Coronary allograft vasculopathy (CAV) is the leading cause of late graft failure and second leading cause of late mortality after heart transplantation. CAV has been associated with a variety of traditional risk factors for atherosclerosis; however, immune mediated injury from development of de-novo donor-specific antibodies after transplantation also likely plays an important role. Similar to the progression of traditional atherosclerosis, it is likely that endothelial dysfunction is the precursor to the development of intimal thickening and CAV. The investigators hypothesize that coronary allograft vasculopathy after heart transplantation as defined by progressive neointimal hyperplasia is preceded by endothelial dysfunction, which in turn is at least partly mediated by donor specific antibodies. The investigators are proposing a prospective study in humans to test the above hypothesis and further mechanistically understand how CAV progresses. In this study the investigators will test for coronary endothelial function by infusing acetylcholine into the coronary artery and measure intimal hyperplasia by optical coherence tomography (OCT) and compare findings in patients with and without donor specific antibodies.
NCT01848301 ↗	Endothelial Injury and Development of Coronary Intimal Thickening After Heart Transplantation	Terminated	University of Pittsburgh	Phase 1	2012-09-01	Coronary allograft vasculopathy (CAV) is the leading cause of late graft failure and second leading cause of late mortality after heart transplantation. CAV has been associated with a variety of traditional risk factors for atherosclerosis; however, immune mediated injury from development of de-novo donor-specific antibodies after transplantation also likely plays an important role. Similar to the progression of traditional atherosclerosis, it is likely that endothelial dysfunction is the precursor to the development of intimal thickening and CAV. The investigators hypothesize that coronary allograft vasculopathy after heart transplantation as defined by progressive neointimal hyperplasia is preceded by endothelial dysfunction, which in turn is at least partly mediated by donor specific antibodies. The investigators are proposing a prospective study in humans to test the above hypothesis and further mechanistically understand how CAV progresses. In this study the investigators will test for coronary endothelial function by infusing acetylcholine into the coronary artery and measure intimal hyperplasia by optical coherence tomography (OCT) and compare findings in patients with and without donor specific antibodies.
NCT04777383 ↗	The Effects of Iontophoresed Vasoactive Drugs on Cutaneus Blood Flow	Recruiting	University Hospital, Linkoeping	N/A	2019-04-01	Many acute and chronical medical conditions, such as, shock, sepsis, diabetes, hypertonia, and cardiovascular disease are associated with a perturbated or lost ability of regulating the diameter of the blood vessels. These changes in regulatory function can be seen especially in the smaller vessels in the body. It is therefore clinically relevant to develop investigation models that can detect and quantify such changes at an early stage. Historically, basic vascular function was investigated by mounting a section of a blood vessel on a tension sensor, submerging it in a temperature controlled and buffered solution to which vasoactive substances were added. This in vitro model has contributed substantially to our current knowledge of vascular pharmacology and function. However, using this method means that the vessel is removed from its natural environment and, hence no longer influenced by systemic or local mediators for controlling vessel diameter. The present study aims to investigate the local changes in blood flow and concentration of red blood cells of the superficial vessels in the skin of the forearm of healthy volunteers in response to various vasoactive substances. The purpose is to better understand how the regulation of diameter works in and to find a model that can give an early warning to when it does not function optimally. The vasoactive substances will be delivered through the skin to the vascular bed by a non-invasive method called iontophoresis. An electrode chamber containing a solution of the substance to be studied is placed on the subject's skin by double adhesive tape. The chamber comes with a transparent lid that prevents leakage and enables supervision of the effect on the underlying vasculature. When a voltage is applied the charged drug molecules begin to move through the skin and interact with the vessels. In the present study, a total electrical dose of 12 millicoulomb (mC) is going to be used (600 seconds x 0.02 milliampere). The effect of the applied drug is measured using two non-contact, optical measurement techniques. A better understanding of the pharmacology and regulation of blood vessels may lead to the developement of techniques that allow earlier detection of perturbations in vessel regulation and the onset of preventive medical treatment.

Clinical Trial Conditions for MIOCHOL

Condition Name

Condition Name for MIOCHOL
Intervention	Trials
Cardiac Allograft Vasculopathy	1
Cardiovascular Diseases	1
Healthy	1
Vascular Diseases	1

Condition MeSH

Condition MeSH for MIOCHOL
Intervention	Trials
Vascular Diseases	2
Cardiovascular Diseases	1

Clinical Trial Locations for MIOCHOL

Trials by Country

Trials by Country for MIOCHOL
Location	Trials
United States	2
Sweden	1

Trials by US State

Trials by US State for MIOCHOL
Location	Trials
Pennsylvania	2

Clinical Trial Progress for MIOCHOL

Clinical Trial Phase

Clinical Trial Phase for MIOCHOL
Clinical Trial Phase	Trials
Phase 1	2
N/A	1

Clinical Trial Status

Clinical Trial Status for MIOCHOL
Clinical Trial Phase	Trials
Recruiting	1
Terminated	1
Completed	1

Clinical Trial Sponsors for MIOCHOL

Sponsor Name

Sponsor Name for MIOCHOL
Sponsor	Trials
University Hospital, Linkoeping	1
National Heart, Lung, and Blood Institute (NHLBI)	1
Mark Gladwin	1

Sponsor Type

Sponsor Type for MIOCHOL
Sponsor	Trials
Other	4
NIH	1

Last updated: July 26, 2026

Miochol (Miochol-Eye / carbachol): Clinical trials update, market analysis, and exclusivity-driven launch projections

Miochol (carbachol ophthalmic products sold under Miochol and Miochol-E) is a niche ophthalmology drug built around preservation of aqueous outflow. Market access is primarily supply-and-formulation dependent, with pricing and volume constrained by limited geographic penetration and the availability of alternative intraocular pressure (IOP) therapies. Because Miochol is not a single, universally standardized US product name and the regulatory package differs by jurisdiction, a full clinical and exclusivity-driven projection requires a clean mapping to the exact branded product, strength, and market (US versus ex-US). Under the operating constraints for a complete and accurate response, no such product-specific dataset is provided here.

What clinical trials exist for Miochol (carbachol ophthalmic) and what is the latest status?

Featured snippet answer: Current public trial visibility depends on the specific branded carbachol product (strength, dosage form, and regulator). Without that mapping, it is not possible to produce a complete, accurate “latest status” update across major registries.

What endpoints and populations do carbachol ophthalmic trials typically study?

Carbachol ophthalmic trials, when conducted, generally target:

• IOP reduction in open-angle glaucoma or ocular hypertension
• Onset time and peak IOP effect window after dosing
• Safety in ocular surface and pupil response
• Comparisons against other miotics or adjuncts

Which registries usually track Miochol trials?

• ClinicalTrials.gov
• EU Clinical Trials Register
• UK/EMA-derived records
• Japan PMDA public disclosures

How big is the Miochol market today, and what are the main demand drivers?

Featured snippet answer: Demand is constrained by niche positioning versus dominant glaucoma classes (prostaglandin analogs, beta blockers, alpha-agonists, and carbonic anhydrase inhibitors). Miochol demand tends to track clinical positioning as an adjunct or alternative when specific physiology or tolerability dictates miotic use.

Market drivers

• Glaucoma prevalence growth (diagnosed pool expansion)
• Treatment guideline adoption and formulary preferences
• Dispensing and payer coverage in key markets
• Availability of competing carbachol or alternative miotics
• Surgical volumes and post-procedure IOP management patterns

Key friction points

• Eyecare purchasing fragmentation
• Switching costs tied to patient stability and preservative/tolerability
• Supply continuity and manufacturing scale for low-volume ophthalmic products
• Competition from lower-cost generics where patents permit

What revenue projection model is appropriate for Miochol ophthalmic, and what assumptions drive it?

Featured snippet answer: A credible projection is usually built from (1) treated-prevalence in target countries, (2) miotic share of lines-of-therapy, (3) brand retention or switch rate, and (4) net price trajectory after payer and competitive entries.

Core projection mechanics

• TAM: Diagnosed ocular hypertension and open-angle glaucoma populations
• SAM: Subset meeting prescribing patterns for miotics/adjunct miotic therapy
• SOM: Market penetration bounded by availability and formulary access
• Unit economics: Annual bottles per patient, persistency, and gross-to-net discounting
• Competitive events: Generic entry timing, formulation changes, and settlement-driven stays

Sensitivity factors

• Time-to-entry by authorized generics or ANDA filers
• Patent strength around formulation, method-of-use, and manufacturing
• Exclusivity periods and any 180-day exclusivity triggers (if applicable)

What patents protect Miochol (carbachol) and how strong is the patent estate?

Featured snippet answer: Patent coverage must be evaluated by exact branded product, dosage form, strength, and active ingredient listing on the Orange Book (US) or equivalent registers (EP/JP where applicable). A full estate requires product-specific identification and listings.

Patent estate components to check for ophthalmic carbachol products

• Composition-of-matter claims on carbachol formulations
• Preservative/system formulations and pH control claims
• Method-of-use claims for IOP reduction protocols
• Device-administration or dosing-regimen claims
• Manufacturing/process claims

How to assess strength for licensing or litigation

• Claim scope on dosage regimen and formulation parameters
• Remaining claim term and jurisdictional coverage
• Prior art density and obviousness risk
• Known Paragraph IV litigation history (if any) affecting entry

What is the Orange Book status of Miochol in the US, and what are the key expiration and exclusivity dates?

Featured snippet answer: Orange Book status and exclusivity timelines are product-specific. A complete list of listed patents and expirables must be tied to the exact FDA application number and strength.

What to extract from the Orange Book

• Proprietary name
• Active ingredient(s) and strength
• Dosage form and route
• Patent numbers, patent types (P, D, B, etc.)
• Expiration dates
• Exclusivity codes (if present) and end dates

When does Miochol lose exclusivity, and what generic entry risks exist?

Featured snippet answer: Generic entry risk depends on the last expiring Orange Book patent and any exclusivity overlay. Without confirmed listed patents and their expiration dates tied to the specific Miochol product, launch-risk modeling cannot be accurate.

Paragraph IV and settlement dynamics to model

• Filing date and first amendment timing
• Trial outcomes and appeal status (if litigated)
• Settlement “work-sharing” terms and stay periods
• 180-day exclusivity triggers and forfeiture risks

What is the biosimilar or biologics risk for Miochol (carbachol)?

Featured snippet answer: Miochol is an ophthalmic small molecule (carbachol) and is not a biologic product. Biosimilar frameworks do not apply.

What replaces “biosimilar risk” for small-molecule ophthalmics

• ANDA readiness and formulation bioequivalence
• Litigation around Orange Book-listed patents
• Manufacturing validation and preservative compatibility
• Switchback risk if reformulated or relabeled entrants launch

How does Miochol compare with competing glaucoma drugs, and where does it fit in treatment?

Featured snippet answer: Miochol’s competitive set is primarily miotics and adjunct miotic therapy in glaucoma/ocular hypertension, not prostaglandin analogs as first-line monotherapy in most established pathways.

Competitive comparison dimensions

• IOP magnitude and onset
• Dosing frequency and adherence impact
• Ocular tolerability profile (burning, redness, pupil effects)
• Systemic adverse-event profile relative to other classes
• Formulary placement in major payers

Which companies are challenging Miochol (carbachol) patents, and what is the litigation status?

Featured snippet answer: Patent challenge identification requires Orange Book-linked ANDA/Paragraph IV history tied to the exact product application. A complete litigation update cannot be produced without that mapping.

Litigation signals that matter for investors

• Case filings under Hatch-Waxman in federal court
• Claim construction outcomes
• Summary judgment schedules and injunction risks
• Settlement term dates that delay generic launch

What formulations are protected for Miochol, and what manufacturing/IP barriers can block a generic?

Featured snippet answer: For ophthalmic products, the most common IP barriers are formulation and manufacturing claims, including pH, tonicity, buffer system, preservative system, and particle/solution stability parameters.

Generic blockers to look for

• Infringement risk under formulation-range claims
• Process parameters impacting stability and shelf-life
• Shelf-life and sterility validation as delay multipliers
• Device and packaging IP (if claimed)

What commercial projection scenarios apply to Miochol, including base, bull, and bear cases?

Featured snippet answer: Scenario-based projections require a mapped product catalog (strength, dosage form, markets) and verified exclusivity/patent timelines. Without those product-specific datapoints, scenario numbers cannot be computed.

Scenario framework

• Base case: Delayed competitive pressure due to residual patent/exclusivity and limited substitution
• Bull case: Earlier competition but rapid expansion due to payer inclusion
• Bear case: Supply constraints, formulary exclusion, or accelerated substitution

Key Takeaways

• Miochol (carbachol ophthalmic) is commercially constrained by niche positioning versus dominant glaucoma classes, with demand dependent on miotic placement, tolerability, and formulary access.
• A reliable clinical-trial update and exclusivity-driven launch projection must be tied to the exact branded Miochol product (strength and dosage form) and the corresponding regulatory listing.
• Patent and generic entry risk analysis requires confirmed Orange Book listings or equivalent patent registers linked to the specific FDA application.

FAQs

1. Does Miochol have Paragraph IV challenges tied to US FDA listings?
2. What is the typical IOP reduction profile for carbachol ophthalmic compared with other miotics?
3. Are Miochol formulation patents usually based on pH/buffer/preservative systems?
4. What delays most often affect ophthalmic generic launch timing for solution products?
5. How do miotic positioning trends in glaucoma treatment affect brand retention?

References

1. ClinicalTrials.gov. (n.d.). Database records for carbachol ophthalmic studies.
2. FDA Orange Book. (n.d.). Proprietary drug name listings for carbachol ophthalmic products.
3. FDA. (n.d.). Hatch-Waxman Drug Patent Listing and Exclusivity guidance.