Intracameral Implants

Number: 1065

Table Of Contents

Policy
Applicable CPT / HCPCS / ICD-10 Codes
Background
References

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Policy

Scope of Policy

This Clinical Policy Bulletin addresses intracameral implants.

1. Prescriber Specialties

   These implants must be prescribed by or in consultation with an ophthalmologist.

2. Criteria for Initial Approval

   1. Bimatoprost (Durysta)

      Aetna considers a one-time intracameral injection of the bimatoprost (Durysta) implant medically necessary for the reduction of intraocular pressure (IOP) in members with open angle glaucoma (OAG) or ocular hypertension (OHT) when all of the following criteria are met:

      1. Member is 18 years of age or older; and
      2. Member has experienced an inadequate treatment response or intolerance to at least one topical ophthalmic prostaglandin (e.g., bimatoprost, lantanoprost, travaprost); and 
      3. Member has experienced an inadequate treatment response, intolerance, or has a contraindication to at least one topical beta-adrenergic blocker (e.g., betaxolol, metipranolol, timolol); and
      4. Durysta will only be administered to the affected eye; and
      5. The affected eye has not received prior treatment with Durysta; and 
      6. Dose does not exceed 10 mcg bimatroprost per affected eye.

      Aetna considers readministration of bimatoprost intracameral implant (Durysta) experimental, investigational, or unproven because the effectiveness of this approach has not been established.

      Aetna considers bimatoprost intracameral implant (Durysta) implantation combined with cataract surgery experimental, investigational, or unproven because the effectiveness of this approach has not been established. 

   2. Travoprost (iDose TR)

      Aetna considers surgical placement of the travoprost (iDose TR) implant medically necessary for the reduction of intraocular pressure (IOP) in members with open angle glaucoma (OAG) or ocular hypertension (OHT) when all of the following criteria are met:

      1. Member is 18 years of age or older; and
      2. Member has experienced an inadequate treatment response or intolerance to at least one topical ophthalmic prostaglandin (e.g., bimatoprost, lantanoprost, travaprost); and
      3. Member has experienced an inadequate treatment response, intolerance, or has a contraindication to at least one topical beta-adrenergic blocker (e.g., betaxolol, metipranolol, timolol); and
      4. Evaluation of the corneal endothelium by specular microscpy and establishing pre-implantation baseline corneal endothelial cell density prior to initial administration of iDose TR and prior to each readministration; and
      5. iDose TR will only be administered to the affected eye; and
      6. Dose does not exceed 75mcg travoprost per affected eye; and
      7. Readministration of iDose TR must not be performed more than once per year.

      Note: iDose TR should be readministered with caution in eyes with 10% or greater loss in central corneal endothelial cell density from pre-administration baseline.

   Aetna considers all other indications as experimental, investigational, or unproven.

3. Related Policies

   1. CPB 0435 - Viscocanalostomy and Canaloplasty
   2. CPB 0484 - Glaucoma Surgery

Dosage and Administration

Durysta

Durysta is an ophthalmic drug delivery system containing 10 mcg of bimatoprost for a single intracameral administration of a biodegradable implant. Each Durysta intracameral implant comes preloaded in a single-use applicator with a 28-gauge needle. The intracameral administration should be carried out under standard aseptic conditions. Durysta should not be re-administered to an eye that received a prior Durysta dose. 

Source: AbbVie, 2024

iDose TR

iDose TR is an ophthalmic drug delivery system consisting of a travoprost releasing implant pre-loaded in a sterile, single-dose inserter. iDose TR contains 75 mcg travoprost administered intracamerally through a small, clear corneal incision and is anchored into the sclera at the iridocorneal angle. The intracameral administration should be carried out under standard aseptic conditions. Perform specular microscopy to evaluate the corneal endothelium and establish pre-implantation baseine corneal endothelial cell density prior to the initial administration of iDose TR and prior to each readministration. It is not recommended to readminister an iDose TR more than once per year.

Note: When readministering an iDose TR implant, always remove the previous iDose TR implant after implantation of the new implant.

Source: Glaukos, 2026

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Table:

CPT Codes / HCPCS Codes / ICD-10 Codes

Code	Code Description
CPT codes not covered for indications listed in the CPB:
Bimatoprost intracameral implant (Durysta) combined with cataract surgery- No specific code
Other CPT codes related to the CPB:
0660T	Implantation of anterior segment intraocular nonbiodegradable drug-eluting system, internal approach
0661T	Removal and reimplantation of anterior segment intraocular nonbiodegradable drug-eluting implant
66030	Injection, anterior chamber of eye (separate procedure); medication
66820-66991	Cataract Surgery
HCPCS codes covered if selection criteria are met:
J7351	Injection, bimatoprost, intracameral implant, 1 microgram
J7355	Injection, travoprost, intracameral implant, 1 microgram
ICD-10 codes covered if selection criteria are met:
H40.051 – H40.059	Ocular hypertension
H40.10X0 - H40.159	Open-angle glaucoma

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Background

U.S. Food and Drug Administration (FDA)-Approved Indications for Durysta

• Durysta (bimatoprost intracameral implant) is a prostaglandin analog indicated for the reduction of intraocular pressure (IOP) in patients with open angle glaucoma (OAG) or ocular hypertension (OHT).

Durysta (AbbVie Inc), a biodegradable intracameral implant, is indicated for IOP control. The implant is composed of a solid polymer matrix designed to hydrolyze and slowly release bimatoprost directly into the anterior chamber of the eye. Bimatoprost, a prostaglandin analog used in anti-glaucoma topical eye drops, is believed to lower IOP (measurement of the fluid pressure inside the study eye) by increasing outflow of aqueous humor through both the trabecular meshwork (conventional) and uveoscleral routes (unconventional). Elevated IOP presents a major risk factor for glaucomatous field loss. The higher the level of IOP, the greater the likelihood of optic nerve damage and visual field loss.

Durysta is preloaded into a single-use applicator for injection into the eye. The procedure is performed under magnification that allows clear visualization of the anterior chamber structures and is carried out using standard aseptic conditions for intracameral procedures, with the patient's head in a stabilized position. Following administration, the intracameral implant is intended to settle within the inferior angle to deliver a sustained release of bimatoprost. Thus, Durysta should be used with caution in patients with narrow iridocorneal angles (Shaffer grade less than 3) or anatomical obstruction (e.g., scarring) that may prohibit settling in the inferior angle.

Durysta implant is designed to last several months. However, due to possible corneal endothelial cell loss, administration of Durysta is limited to a single implant per eye without retreatment. Thus, a one-time only administration per affected eye. 

Durysta was approved by the FDA in March 2020 as the first biodegradable sustained-release intracameral implant indicated for the treatment of OAG or OHT. Approval was based on the efficacy results of two multicenter, randomized, parallel-group, phase 3 studies (ARTEMIS) which evaluated the implant over 20 months, including an 8-month extended follow up. The studies compared Durysta to twice daily topical timolol 0.5% drops in 1122 patients with OAG or OHT. The primary efficacy endpoint was IOP in the study eye at Hours 0 and 2 at Weeks 2, 6, and 12. Durysta demonstrated an IOP reduction of approximately 5-8 mmHg (30%) in patients with a mean baseline IOP of 24.5 mmHg over the 12-week primary efficacy period, meeting the predefined criteria for non-inferiority compared to timolol. Durysta was not administered in both eyes of any patient in the clinical studies. 

In a randomized, 20-month, multicenter, masked, parallel-group, phase 3 trial, Bacharach et al (2021) evaluated the IOP-lowering efficacy and safety of 10 and 15 µg bimatoprost implant in patients with OAG or OHT. The trial enrolled 528 patients with OAG or OHT and an open iridocorneal angle inferiorly. Study eyes were administered 10 or 15 µg bimatoprost implant on day 1, week 16, and week 32, or twice-daily topical timolol maleate 0.5%. Primary endpoints were IOP and IOP change from baseline through week 12. Safety measures included treatment-emergent adverse events (TEAEs) and corneal endothelial cell density (CECD). Both 10 and 15 µg bimatoprost implant met the primary endpoint of non-inferiority to timolol in IOP lowering through 12 weeks. Mean IOP reductions from baseline ranged from 6.2-7.4, 6.5-7.8, and 6.1-6.7 mmHg through week 12 in the 10 µg implant, 15 µg implant, and timolol groups, respectively. IOP lowering was similar after the second and third implant administrations. Probabilities of requiring no IOP-lowering treatment for 1 year after the third administration were 77.5% (10 µg implant) and 79.0% (15 µg implant). The most common TEAE was conjunctival hyperemia, typically temporally associated with the administration procedure. Corneal TEAEs of interest (primarily corneal endothelial cell loss, corneal edema, and corneal touch) were more frequent with the 15 than the 10 µg implant and generally were reported after repeated administrations. Loss in mean CECD from baseline to month 20 was ~ 5% in 10 µg implant-treated eyes and ~ 1% in topical timolol-treated eyes. Visual field progression (change in the mean deviation from baseline) was reduced in the 10 µg implant group compared with the timolol group. The authors concluded that the results corroborated the previous phase 3 study of the bimatoprost implant. The bimatoprost implant met the primary endpoint and effectively lowered IOP. The majority of patients required no additional treatment for 12 months after the third administration. The benefit-risk assessment favored the 10 over the 15 µg implant. Studies evaluating other administration regimens with reduced risk of corneal events are ongoing. The authors state that the bimatoprost implant has the potential to improve adherence and reduce treatment burden in glaucoma. 

The authors acknowledged some study limitations. One study limitation may have been the requirement for implant administrations at a fixed 4-month interval, because many patients may have had adequate IOP control and not needed repeated administrations. The authors note that this issue is being addressed by the ongoing studies that are evaluating an as-needed dosing regimen. An additional limitation is that the Kaplan-Meier analysis was an indirect measure of the maintenance of the IOP-lowering effect over time. The decision of when to rescue was up to the investigator, and there were no defined IOP criteria for rescue. Nonetheless, the implant effectively lowered IOP, and in many patients the IOP control provided by the implant persisted beyond the expected duration of intraocular drug bioavailability. Ongoing studies are evaluating 24-h IOP control with the bimatoprost implant and the effects of the implant on the visual field. Studies are also in progress to understand ideal treatment intervals, given the unexpectedly long duration of action of the implant.

Medeiros et al (2022) evaluated the IOP-lowering efficacy and safety of a single intracameral administration of bimatoprost implant 10 µg in adults with OAG or OHT. Two identically designed, randomized, 20-month, parallel-group, phase 3 clinical trials (one study eye/patient) compared three administrations of 10- or 15-µg bimatoprost implant (day 1, weeks 16 and 32) with twice-daily topical timolol maleate 0.5%. An open-label, 24-month, phase 1/2 clinical trial compared one or two implants administered in the study eye with once-daily topical bimatoprost 0.03% in the fellow eye. Separate analyses of the pooled phase 3 and phase 1/2 study datasets evaluated outcomes in the 10-µg bimatoprost implant and comparator treatment arms after a single implant administration, up to the time of implant re-administration or rescue with IOP-lowering medication. In the phase 3 studies, 10-µg bimatoprost implant single administration demonstrated IOP reductions (hour 0) of 4.9-7.0 mmHg through week 15 from a mean (standard deviation, SD) baseline IOP of 24.5 (2.6) mmHg (n = 374); IOP in the topical timolol BID group was reduced by 6.0-6.3 mmHg from a mean (SD) baseline IOP of 24.5 (2.6) mmHg (n = 373). In the phase 1/2 study (n = 21), median time to use of additional IOP-lowering treatment (Kaplan-Meier analysis) was 273 days (approximately 9 months), and 5 of 21 enrolled patients (23.8%) required no additional IOP-lowering treatment up to 24 months after single administration. In each study, after a single implant administration there were no reports of corneal edema, corneal endothelial cell loss, or corneal touch, and no patients had 20% or greater loss in corneal endothelial cell density. The authors concluded that a single administration of bimatoprost implant lowers IOP and has shown a favorable safety profile. However, additional studies are needed to further evaluate the duration of effect and factors predicting long-term IOP lowering after a single implant administration.

Weinreb and colleagues (2023) evaluated the degree of biodegradation of the bimatoprost implant over time in the phase 3 ARTEMIS studies. A secondary objective was to evaluate the morphology of the implant during biodegradation in a preclinical study. In 2 identically designed, randomized, phase 3 clinical trials, adults with OAG or OHT and open iridocorneal angles inferiorly in the study eye were administered 10- or 15-μg bimatoprost implant (day 1 and weeks 16 and 32) or twice-daily topical timolol 0.5%. Implants were assessed on gonioscopy throughout the studies. Investigators reported whether implants were visible, estimated the size of visible implants relative to their initial size at implantation, and reported the implant location. Data for 10-μg implant placed on day 1 were pooled from both studies for analysis. A total of 372 patients received the 10-μg bimatoprost implant. The degree of implant biodegradation at each follow-up time point was variable among patients. The implant frequently swelled during the initial phase of biodegradation from 6 to 28 weeks. Accelerated biodegradation occurred between 31 and 52 weeks, resulting in 82% of implants absent or less than or equal to 25% of initial size by 52 weeks. By month 20, 95% of implants had biodegraded to absent or less than or equal to 25% of initial size. The implant was predominantly located inferiorly in the iridocorneal angle. The authors concluded that the bimatoprost implant biodegradation in the studies showed some degree of variability among patients, and clinically significant implant biodegradation was observed in the majority of patients by 12 months. However, clinical studies are in progress to further understand implant biodegradation and the ideal timing for implant re-administration.

The authors acknowledged that corneal adverse events occurred in the ARTEMIS studies when 10- or 15-μg bimatoprost implant was re-administered at 16-week intervals, with a higher incidence of these events associated with the larger 15-μg implant. Consequently, a single administration per eye of the smaller 10-μg bimatoprost implant is currently indicated to lower IOP in patients with open-angle glaucoma or ocular hypertension. However, the long duration of IOP lowering frequently observed after implant administration suggests the potential for safe and effective re-administration of the implant using a longer dosing interval. Ongoing, open-label clinical studies (NCT03850782, NCT03891446) are evaluating the safety and efficacy of as-needed administration of the implant.

Durysta is contraindicated in patients with: active or suspected ocular or periocular infections; corneal endothelial cell dystrophy (e.g., Fuchs’ Dystrophy); prior corneal transplantation or endothelial cell transplants (e.g., Descemet’s Stripping Automated Endothelial Keratoplasty [DSAEK]); absent or ruptured posterior lens capsule, due to the risk of implant migration into the posterior segment; and hypersensitivity to bimatoprost or to any other components of the product.

Durysta has been associated with corneal adverse reactions and risks are increased with multiple implants. The label cautions use in patients with limited corneal endothelial cell reserve, as well as in patients with narrow angles or anatomical angle obstruction.

The most common ocular adverse reaction reported by 27% of patients was conjunctival hyperemia. Other common adverse reactions reported in 5-10% of patients were foreign body sensation, eye pain, photophobia, conjunctival hemorrhage, dry eye, eye irritation, intraocular pressure increased, corneal endothelial cell loss, vision blurred, iritis, and headache. 

Mann et al (2025) noted that bimatoprost implant 10-µg (Durysta) is an intra-cameral biodegradable implant that releases bimatoprost to lower IOP.  In a prospective, observational, open-label, 18-month, multi-center, phase-IV clinical trial (The ARGOS Trial), these investigators examined the safety and effectiveness of the implant in patients with OAG or OHT.  This study enrolled adult patients with OAG or OHT who were scheduled to receive the bimatoprost implant in 1 or both eyes.  Data collected included IOP, use of topical IOP-lowering medications, treatment-emergent AEs (TEAEs), and CECD.  The primary end-point was the proportion of primary (1st-treated) eyes that received no additional (new) IOP-lowering treatment per standard medical care through month 6 following the implant administration.  A total of 217 patients (341 eyes) were enrolled, and 132 patients (60.8 %) and 203 eyes (59.5 %) completed the study.  Most patients were on topical IOP-lowering medication before receiving the implant.  After implant administration, the proportion of primary eyes that had received no additional treatment was 88.6 % (95 % CI: 86.6 to 90.6) at month 6 (primary end-point) and remained high throughout the follow-up: 83.7 % (95 % CI: 80.2 to 87.3) at month 12 and 77.7 % (95 % CI:73.4 to 82.1) at month 18.  IOP was reduced after implant administration, with mean changes in IOP from baseline at follow-up visits ranging from - 1.0 to - 2.0 mm Hg.  The mean number of topical IOP-lowering medications used was also reduced, from 1.8 at baseline to 0.9 at month 12, and 1.0 at month 18.  Increased IOP and dry eye were the most common ocular TEAEs.  The mean percentage change in CECD from baseline at month 18 (central reading center evaluation) was - 3.47 %.  In qualitative interviews, most patients (84 %, 21/25) reported overall satisfaction with their treatment outcomes.  The authors concluded that the bimatoprost implant aided in controlling IOP and reducing topical medication use.  Throughout the 18 months after implant administration, an estimated 77.7 % of eyes needed no new added medication for IOP management.  Additionally, patient-reported outcomes (PROs) were favorable, and the safety profile of the implant was acceptable.

Silverstein et al (2025) stated that bimatoprost implant 10-µg is an intra-cameral, biodegradable implant that slowly releases bimatoprost to lower IOP.  In a phase-IIIb clinical trial (The TRITON Trial), these researchers examined the safety and the duration of the IOP-lowering effect after single and as-needed repeat administration of the bimatoprost implant in patients with OAG and OHT.  This study was an interim analysis of an ongoing, prospective, open-label, multi-center study in patients with OAG or OHT who are inadequately managed with topical IOP-lowering medication for reasons other than efficacy.  IOP-lowering rescue treatment was allowed if implant re-treatment criteria were not met.  The primary end-point was time to re-treatment/rescue following the initial implant administration analyzed with the Kaplan-Meier method.  Key safety measures include TEAEs and reading-center evaluation of CECD.  Analysis of data collected through September 15, 2023 focused on outcomes after 1 or 2 implant(s).  A total of 441 patients received the 10-µg bimatoprost implant in the study eye on day 1 (cycle 1), 179 patients received a 2nd administration (cycle 2), and 378 patients had at least 12 months of follow-up data available.  The median time (95 % CI) from the 1st administration to a 2nd administration or rescue was 392 days (369 to 485); the probability of not requiring re-treatment or rescue by day 360 was 57.5 %.  A 2nd implant administration similarly provided a long duration of IOP control.  The baseline mean (standard error, SE) IOP was 25.6 (0.14) mmHg; the mean (SE) change from baseline IOP in un-rescued eyes after a single administration was - 7.5 (0.21) mmHg at week 24 and - 6.4 (0.28) mmHg at month 12.  Conjunctival hyperemia, typically associated with the administration procedure, was the most common ocular TEAE (cycle 1, 14.3 %; cycle 2, 12.8 %).  Mean (SE) percentage change in CECD from baseline at 12 months after administration was - 4.3 (0.81) % in cycle 1, and - 8.5 (2.22) % in cycle 2.  The cycle 1 implant was no longer visible or 25 % or less of initial size in 66.3 % and 94.3 % of study eyes at months 12 and 24, respectively.  The authors concluded that in this interim analysis based on available data, the IOP-lowering effect of the initial administration of the 10-µg bimatoprost implant was well-maintained for more than 1 year in most patients; and results after a 2nd administration were comparable.  Moreover, the safety profile of initial and repeat administration was acceptable.

The safety and efficacy has not been established in pediatric patients.

U.S. Food and Drug Administration (FDA)-Approved Indications for iDose TR

• iDose TR (travoprost intracameral implant) is a prostaglandin analog indicated for the reduction of intraocular pressure (IOP) in patients with open-angle glaucoma (OAG) or ocular hypertension (OHT).

iDose TR (Glaukos Corporation) is a sterile intracameral implant containing 75 mcg of travoprost. The intracameral implant consists of a titanium implant reservoir with a membrane controlling the sustained release of travoprost. The sterile implant is pre-loaded in a sterile single-dose inserter to facilitate insertion directly through the trabecular meshwork of the anterior chamber angle into the sclera. Travoprost, a prostaglandin analog used in anti-glaucoma topical eye drops, is believed to reduce IOP by increasing uveoscleral outflow. The exact mechanism of action is unknown at this time. iDose TR is surgically placed intracamerally through a small, clear corneal incision and is anchored into the sclera at the iridocorneal angle. iDose TR should not be re-administered to an eye that received a prior iDose TR. If the iDose TR implant becomes dislocated, it should be surgically removed.

In December 2023, the FDA approved a single administration, per eye, of iDose TR for reduction of IOP in patients with OHT or OAG. Approval was based on results from two multicenter, 12-month, randomized, parallel-group, double-masked, controlled clinical trials in patients with OAG or OHT. In both trials (GC-010, NCT03519386, and GC012, NCT03868124), iDose TR was compared to twice-daily topical administration of timolol maleate ophthalmic solution, 0.5%. In the first 3 months following administration, iDose TR demonstrated an IOP change from baseline of -6.6 to -8.4 mmHg in the study eye of patients with a mean baseline IOP of 24 mmHg. iDose TR demonstrated non-inferiority to timolol ophthalmic solution in IOP reduction during the first 3 months. Subsequently, iDose TR did not demonstrate non-inferiority over the next 9 months.

In a multicenter, randomized, double-masked, sham-controlled, non-inferiority trial, Sarkisian et al (2024a) evaluated the safety and IOP-lowering efficacy of 2 models of the travoprost intraocular implant (fast-eluting [FE] and slow-eluting [SE] types) from 1 of 2 phase 3 trials (the GC-010 trial) in patients with OAG or OHT. Study eyes were randomized to the travoprost intraocular implant (FE implant [n = 200] or SE implant [n = 197] model) or to timolol ophthalmic solution 0.5% twice daily (n = 193). The primary outcome was mean change from baseline IOP in the study eye at 8 am and 10 am, at each of day 10, week 6, and month 3. Safety outcomes included adverse events (AEs) and ophthalmic assessments. Mean IOP reduction from baseline over the 6 time points ranged from 6.6 to 8.4 mmHg for the FE implant group, from 6.6 to 8.5 mmHg for the SE implant group, and from 6.5 to 7.7 mmHg for the timolol group. The primary efficacy end point was met; the upper limit of the 95% confidence interval of the difference between the implant groups and the timolol group was less than 1 mmHg at all 6 time points. Study eye AEs, most of mild or moderate severity, were reported in 21.5%, 27.2%, and 10.8% of patients in the FE implant, SE implant, and timolol groups, respectively. The most common AEs included iritis (FE implant, 0.5%; SE implant, 5.1%), ocular hyperemia (FE implant, 3.0%; SE implant, 2.6%), reduced visual acuity (FE implant, 1.0%; SE implant, 4.1%; timolol, 0.5%), and IOP increased (FE implant, 3.5%; SE implant, 2.6%; timolol, 2.1%). One serious study eye AE occurred (endophthalmitis). The authors concluded that the travoprost intraocular implant demonstrated robust IOP reduction over the 3-month primary efficacy evaluation period after a single administration. The IOP-lowering efficacy in both implant groups was statistically and clinically non-inferior to that in the timolol group, with a favorable safety profile.

Sarkisian and colleagues (2024b) prospectively evaluated the efficacy and safety of the travoprost intracameral SE-implant (slow-eluting implant, the intended commercial product) and FE-implant (fast-eluting implant, included primarily for masking purposes) compared to twice-daily (BID) timolol ophthalmic solution, 0.5% in patients with OAG or OHT. This multicenter, randomized, double-masked pivotal phase 3 trial included adult patients with OAG or OHT who had an unmedicated mean diurnal intraocular pressure (IOP) of 21 or more and unmedicated IOP less than or equal to 36 mmHg at each diurnal timepoint (8 A.M., 10 A.M., and 4 P.M.) at baseline. The eligible eye of each patient was administered an SE-implant, an FE-implant or had a sham administration procedure. Patients who received an implant were provided placebo eye drops to be administered BID and patients who had the sham procedure were provided timolol eye drops to be administered BID. The primary efficacy endpoint, for which the study was powered, was mean change from baseline IOP at 8 A.M. and 10 A.M. at day 10, week 6, and month 3. Non-inferiority was achieved if the upper 95% confidence interval (CI) on the difference in IOP change from baseline (implant minus timolol) was less than 1.5 mmHg at all six timepoints and less than 1 mmHg at three or more timepoints. The key secondary endpoint was mean change from baseline IOP at 8 A.M. and 10 A.M. at month 12. Non-inferiority at month 12 was achieved if the upper 95% CI was less than 1.5 mmHg at both timepoints. Safety outcomes included treatment-emergent adverse events (TEAEs) and ophthalmic assessments. In the study, a total of 590 patients were enrolled at 45 sites and randomized to one of three treatment groups: 197 SE-implant (the intended commercial product), 200 FE-implant, and 193 timolol. The study found that the SE-implant was non-inferior to timolol eye drops in IOP lowering over the first 3 months, and was also non-inferior to timolol at months 6, 9, and 12. The FE-implant was non-inferior to timolol over the first 3 months, and also at months 6 and 9. Of those patients who were on glaucoma medication at screening, a significantly greater proportion of patients in the SE- and FE-implant groups (83.5% and 78.7%, respectively) compared to the timolol group (23.9%) were on fewer topical glaucoma medications at month 12 compared to screening (P < 0.0001, chi-square test). TEAEs, mostly mild, were reported in the study eyes of 39.5% of patients in the SE-implant group, 34.0% of patients in the FE-implant group and 20.1% of patients in the timolol group. The authors concluded that the SE-travoprost intracameral implant demonstrated non-inferiority to timolol over 12 months; whereas, the FE-implant demonstrated non-inferiority over 9 months. Both implant models were safe and effective in IOP lowering in patients with OAG or OHT.

Per the label, iDose TR is contraindicated in ocular or periocular infections; corneal endothelial dystrophy (e.g., Fuch’s Dystrophy, corneal guttatae); prior corneal transplantation or endothelial cell transplants
(e.g., Descemet’s Stripping Automated Endothelial Keratoplasty [DSAEK]); and hypersensitivity to travoprost or any components of the product. Increased pigmentation of the iris can occur. Iris pigmentation is likely to be permanent.

iDose TR should be used with caution in patients with narrow iridocorneal angles (Shaffer grade less than 3) or other angle abnormalities (e.g., peripheral anterior synechia, rubeosis iridis) that could impair proper placement of iDose TR at the planned implantation site. 

Dislocation of the iDose TR has been observed in clinical trials. Patients should be routinely monitored to confirm the location of the iDose TR at the site of administration. If the iDose TR implant becomes
dislocated, it should be surgically removed.

Macular edema, including cystoid macular edema, has been reported during treatment with ophthalmic travoprost, including iDose TR intracameral implant. iDose TR should be used with caution in aphakic patients, in pseudophakic patients with a torn posterior lens capsule, or in patients with known risk factors for macular edema.

Prostaglandin analogs, including iDose TR, have been reported to cause intraocular inflammation. iDose TR should be used with caution in patients with active intraocular inflammation (e.g., uveitis) because the inflammation may be exacerbated.

In controlled studies, the most common ocular adverse reactions reported in 2% to 6% of patients were increases in intraocular pressure, iritis, dry eye, and visual field defects.

iDose TR is MR Conditional. Patients should be informed that the implant is MR Conditional (as noted on their Patient ID card). If the patient requires magnetic resonance imaging (MRI), they should inform their healthcare provider that they have an iDose TR implanted in their eye. A patient with the iDose TR may be safely scanned per the parameters and conditions of use described in the Full Prescribing Information for iDose TR. 

There are no adequate and well-controlled studies of iDose TR administration in pregnant women, the breastfed child, or milk production to inform a drug-associated risk. 

The safety and effectiveness of iDose TR have not been established in pediatric patients.

Intracameral Bimatoprost Implant versus Selective Laser Trabeculoplasty

In a randomized, 24-month, patient- and efficacy evaluator-masked, paired-eye, multi-center, phase-III clinical trial,  Kolko et al (2025) examined the IOP-lowering effect and safety of up to 2 bimatoprost implant administrations versus selective laser trabeculoplasty (SLT).  Subjects were 183 patients with OAG or OHT inadequately managed with topical IOP-lowering medication for reasons other than efficacy.  Patients received a single 360° SLT procedure in 1 eye and 10-µg bimatoprost implant administration in the contralateral eye.  Initially, implant-treated eyes received a 2nd implant at week 16 if safety criteria were met.  After a protocol amendment, implant-treated eyes were re-treated with flexible scheduling if IOP was greater than 17 mm Hg and safety criteria were met.  The primary effectiveness variable was IOP change from baseline, with primary time-points at weeks 4, 12, and 24.  Safety measures included TEAEs and ocular safety measures.  Mean (± SE) baseline IOP (mm Hg) was 25.2 ± 0.22 and 25.1 ± 0.22 in implant- and SLT-treated eyes, respectively.  Least-squares mean (± SE) IOP reduction from baseline (mm Hg) for eyes treated with up to 2 implants versus SLT was 6.8 ± 0.28 versus 6.2 ± 0.28 at week 4, 6.9 ± 0.30 versus 6.4 ± 0.30 at week 12, and 6.9 ± 0.27 versus 6.5 ± 0.28 at week 24.  The probability of not having required non-study (rescue) IOP-lowering treatment at days 360 and 720, respectively, was 67.5 % and 50.2 % for implant-treated eyes versus 68.7 % and 60.6 % for SLT-treated eyes.  The most common ocular TEAE in both implant- and SLT-treated eyes was increased IOP attributed to wearing off of efficacy.  Mean (± SE) percentage change in CECD from baseline at month 24 was -6.2 ± 1.13 % in implant-treated eyes (-7.9 % ± 2.04 % with fixed re-administration; -5.2 % ± 1.35 % with flexible re-administration) versus -3.1 % ± 0.43 % in SLT-treated eyes.  The authors concluded that the bimatoprost implant showed statistical and clinical non-inferiority to SLT in IOP reduction from baseline at weeks 4, 12, and 24.  In subgroup analysis, patients with flexible implant re-administration met the same criteria.  Both the implant and SLT revealed sustained (2-year) IOP lowering in many eyes.  A flexible administration schedule improved the safety profile of the implant over the fixed administration schedule.

Travoprost Intracameral Implantation Combined with Cataract Surgery

Singh et al (2025) noted that the travoprost intracameral implant and cataract surgery both lower IOP.  In a prospective, 12-month, open-label, single-arm study, these researchers examined the safety and IOP-lowering effect at 3 months following administration of travoprost intracameral implant in combination with cataract surgery.  These investigators enrolled patients with age-related cataracts and OAG or OHT in the same eye.  At baseline, patients were required to have an unmedicated mean diurnal IOP (average of 8:00 am, 10:00 am, and 4:00 pm IOPs) of 24 mmHg or greater, and an IOP of 36 mmHg or less at each of these 3 time-points.  On the day of the combined procedure (day 1), patients who had uncomplicated phaco-emulsification cataract surgery received a travoprost intracameral implant.  Follow-up evaluations occurred on day 2 to 3, week 2, week 6, and month 3 visits.  A total of 60 patients had uncomplicated cataract surgery and received a travoprost intracameral implant.  There were no serious AEs.  Study eye AEs were reported in 8.3 % of patients.  The most frequently reported AE was dry eye (6.7 %).  At month 3, the mean diurnal IOP change from baseline was -10.6 mmHg (95 % CI: -11.2 to -9.9; p < 0.0001) from an unmedicated baseline mean diurnal IOP of 25.2 mmHg.  Furthermore, at month 3, 97 % of eyes had a 20 % or greater mean diurnal IOP reduction from baseline, and 91.0 % of eyes had a mean diurnal IOP of 18 mmHg or less.  The authors concluded that administration of a travoprost intracameral implant combined with routine cataract surgery was safe.  The sizable -10.6 mmHg IOP change from baseline at month 3 was both statistically significant and clinically relevant.

The authors stated that this study had several drawbacks.  First, this trial was designed as a single-arm, open-label study given the inherent difficulty in masking the surgeon and the observer performing safety assessments (e.g., gonioscopy, ophthalmoscopy, and slit-lamp biomicroscopy).  Second, the study was carried out at a single center; however, surgeries were carried out by 4 different experienced surgeons.  Third, all patients were White which is not fully representative of the demographic of patients with OAG and may have decreased the likelihood of observing post-operative safety findings since studies have shown that Black race is associated with a higher risk of post-operative IOP spike following cataract surgery, and the study included only a single patient with diabetes mellitus, a co-morbidity associated with increased risk of persistent post-operative inflammation.  Fourth, although a clinical examination was conducted at month 3, a more detailed evaluation of the macula via optical coherence tomography (OCT) or fluorescein angiography (FA) was not performed.  However, no patient presented with decreased or blurred vision suggestive of pseudophakic cystoid macular edema (CME).  Fifth, the lack of endothelial cell density (ECD) measurement at the month 3 visit.  Cataract surgery has been reported to result in a loss of ECD, with the most substantial decline (11.6 %) occurring within the first 3 months post-operatively.  A substantially smaller decline (1.9 %) has been observed 3 months following administration of the travoprost intracameral implant.  Sixth, the current analysis was only 3 months in duration.  However, the study remains ongoing through 12 months to determine the longer-term safety and effectiveness of administering the travoprost intracameral implant in conjunction with cataract surgery.

Intracameral Anesthetic Mydriatic Versus Topical Mydriasis in Pediatric Cataract Surgery

In a randomized, masked, fellow eye-controlled study, Sukhija et al (2024) compared pupil dynamics following the use of pre-mixed intracameral anesthetic mydriatic combination (ICAM) of phenylephrine (0.31 %), tropicamide (0.02 %), and lidocaine (1 %) versus topical mydriatic (TM) drops consisting of tropicamide 0.8 %, phenylephrine 5 %, and cyclopentolate 0.5 % in pediatric cataract surgery.  Participant included children 12 years of age or younger with bilateral cataracts planned for surgery.  One eye was randomized to receive ICAM and the other eye (control) received TM drops.  Commercially available ICAM that was injected at the beginning of surgery or TM 3 times at an interval of 30 mins, 1 hour before the scheduled time of surgery.  The other treatment was administered for the 2nd eye cataract surgery.  Main outcome measure was pupil dynamics at various points of surgery by a masked observer.  A total of 63 patients (126 eyes) were randomized to receive ICAM in 1 eye (group 1) or TM drops (group 2).  The mean age of the children in the study was 15.7 ± 24.3 months (range of 3 months to 5 years).  Adequate mydriasis with a single injection was achieved in 93.5 % of patients in group 1 and 88.8 % of patients in group 2 without additional pharmacotherapy or intervention.  The mean pupillary diameter increased from 1.78 mm to 5.1 mm after injection of 1 unit of ICAM and from 1.75 mm to 6.06 mm with TM drops (p < 0.0001).  The maximum pupillary dilation achieved was 6.06 ± 1.17 mm in group 1 and 6.75 ± 1.07 mm in group 2 (p = 0.004).  The average change in pupillary size from injection of drug until the end of surgery was positive in group 1 (0.75 ± 0.98 mm) and negative in group 2 (-0.3348 ± 2.57 mm), i.e., there was a relative miosis in group 2 toward the end of surgery (p = 0.001).  The authors concluded that topical drugs achieved a larger maximum pupil size compared with ICAM; however, ICAM provided adequate and stable mydriasis without the need for augmentation compared with topical drops in children undergoing cataract surgery.

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References