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A Glaucoma Eye Drop Designed to Protect the Optic Nerve Is Already in Phase II Trials · Glaucoma, Vision & Longevity: Supplements & Science

• 0:00
  SPEAKER_00: A glaucoma eye drop designed to protect the optic nerve is already in phase two trials.
• 0:05
  SPEAKER_00: Status Reviewed, September 4, 2026.
• 0:09
  SPEAKER_00: Introduction.
• 0:10
  SPEAKER_00: Glaucoma treatment has one major limitation.
• 0:13
  SPEAKER_00: Lowering intraocular pressure protects the eye indirectly, but it does not directly repair or support retinal ganglion cells.
• 0:20
  SPEAKER_00: Some patients continue to lose retinal nerve fibers and visual field despite apparently acceptable pressure control.
• 0:27
  SPEAKER_00: G01 eye drops are designed to address that gap.
• 0:30
  SPEAKER_00: The active ingredient is described as recombinant human nerve growth factor variant 2, or RHNGF V2.
• 0:38
  SPEAKER_00: The drug is being tested in a randomized phase 2 trial in people with progressing primary open-angle glaucoma whose intraocular pressure is already controlled.
• 0:48
  SPEAKER_00: The central question is whether a protein placed on the eye's surface can reach the retina and optic nerve in a sufficient amount to keep stressed retinal ganglion cells alive, restore function to damaged but living cells, stabilize retinal nerve fiber and ganglion cell layers, or, more ambitiously, regenerate damaged optic nerve connections.
• 1:08
  SPEAKER_00: The short answer is G01 is biologically plausible as a neuroprotective and possibly neuro-enhancing treatment.
• 1:16
  SPEAKER_00: Genuine optic nerve regeneration is much less established.
• 1:20
  SPEAKER_00: The largest unresolved problem is whether enough of the drug reaches the posterior eye after topical dosing.
• 1:26
  SPEAKER_00: The evidence is promising but uneven.
• 1:29
  SPEAKER_00: Much of the strongest evidence comes from animal models and a small human case series.
• 1:34
  SPEAKER_00: A previous randomized trial of conventional recombinant human nerve growth factor was safe, but did not show statistically significant short-term improvement.
• 1:44
  SPEAKER_00: G01 may be more potent because it is a modified molecule, but that remains unproven in humans.
• 1:51
  SPEAKER_00: The current phase 2 G01 trial.
• 1:54
  SPEAKER_00: The study is registered as NCT0777861, titled A Randomized Double Masked Placebo-Controlled Phase 2 Clinical Trial, Evaluating the Efficacy and Safety of G01 eye drops in the treatment of optic nerve injury associated with open-angle glaucoma.
• 2:10
  SPEAKER_00: It is being sponsored by Qingdao Wanming Biocell Pharmaceutics Co.
• 2:14
  SPEAKER_00: Leted in China.
• 2:15
  SPEAKER_00: The trial began enrolling on March 18, 2026.
• 2:19
  SPEAKER_00: The registry lists an estimated 90 participants, with primary completion expected on October 1, 2027, and overall study completion on December 1, 2027.
• 2:31
  SPEAKER_00: No results had been posted as of September 4, 2026.
• 2:35
  SPEAKER_00: Gier 1 trial record, trial design.
• 2:37
  SPEAKER_00: For the full table, please open this article on VisualFieldtest.com.
• 2:41
  SPEAKER_00: The public registry lists two active concentrations and a placebo.
• 2:46
  SPEAKER_00: Its summary formatting is not entirely consistent about the number of groups, but the intervention listing clearly describes two active dose arms plus a match placebo arm.
• 2:56
  SPEAKER_00: The precise allocation ratio is not stated in the accessible public record.
• 3:01
  SPEAKER_00: G01 trial record.
• 3:03
  SPEAKER_00: Who can enter the study?
• 3:05
  SPEAKER_00: The trial is designed for people with active, measurable glaucoma progression, not simply people with an abnormal optic nerve.
• 3:12
  SPEAKER_00: Key inclusion criteria include primary open angle glaucoma in one or both eyes.
• 3:18
  SPEAKER_00: Progression in the study eye demonstrated by guided progression analysis of visual field tests.
• 3:23
  SPEAKER_00: Visual field mean deviation between minus 3 and minus 16 decibels.
• 3:28
  SPEAKER_00: Best corrected visual acuity of at least 0.3 in decibel notation.
• 3:33
  SPEAKER_00: Intraocular pressure between 10 and 21 mm of mercury with pressure considered stable by the investigator.
• 3:40
  SPEAKER_00: Ability to attend visits, follow the protocol, and provide informed consent.
• 3:45
  SPEAKER_00: Agreement to use effective contraception when applicable.
• 3:48
  SPEAKER_00: The mean deviation range is important.
• 3:51
  SPEAKER_00: A value closer to zero represents better visual field function.
• 3:55
  SPEAKER_00: A value of minus 16 decibels represents substantially more damage than minus 3 decibels.
• 4:01
  SPEAKER_00: However, the trial excludes many patients with end-stage glaucoma, especially those with mean deviation worse than minus 16 decibels, or only a small central island of remaining vision.
• 4:12
  SPEAKER_00: GO1 trial record.
• 4:14
  SPEAKER_00: Major exclusion criteria.
• 4:16
  SPEAKER_00: The public protocol excludes patients with angle closure, secondary, or inflammatory forms of glaucoma, ocular hypertension without established glaucoma, active or recently active herpes keratitis, significant infection, uveitis, keratitis, endothermitis, or other ocular inflammation, retinal disease, pathological myopia, diabetic retinopathy, retinal vascular occlusion, retinal detachment, retinitis pigmentosa, or another optic neuropathy that could affect the measurements.
• 4:44
  SPEAKER_00: Severe macular or optic nerve disease unrelated to glaucoma.
• 4:48
  SPEAKER_00: Monocular status.
• 4:50
  SPEAKER_00: Recent corneal surgery, intraocular surgery, ocular trauma, laser trabeculoplasty, or glaucoma filtering surgery.
• 4:58
  SPEAKER_00: Conditions that make intraocular pressure measurement unreliable.
• 5:01
  SPEAKER_00: Known allergy to the study drug or placebo.
• 5:04
  SPEAKER_00: Recent or ongoing treatment with other potentially neuroprotective agents, including bromonidine, cytocline, nicotinamide, coenzyme Q, ginkobiloba extract, mycobalamin, other nerve growth factor products, and certain biological preparations, systemic corticosteroids or other immunosuppressive medications, poorly controlled diabetes, severe cardiovascular disease, severe liver or kidney disease, or significant blood disorders, active malignancy or ongoing chemotherapy, pregnancy or breastfeeding, heavy cigarette or alcohol use, recent drug dependence, or participation in another clinical trial.
• 5:41
  SPEAKER_00: These exclusions make scientific sense because they reduce competing causes of visual field change.
• 5:47
  SPEAKER_00: However, they also mean the study will not tell us whether GO1 works in combination with nicotinamide, bromonidine, cytokine, or other neuroprotective therapies.
• 5:58
  SPEAKER_00: GO1 trial record.
• 6:00
  SPEAKER_00: What the trial will measure.
• 6:01
  SPEAKER_00: Primary endpoint, visual field mean deviation.
• 6:05
  SPEAKER_00: The primary endpoint is the change from baseline in visual field mean deviation at day 168, corresponding to approximately 24 weeks of treatment.
• 6:15
  SPEAKER_00: Mean deviation is a summary score from automated visual field testing.
• 6:19
  SPEAKER_00: A worsening score generally indicates loss of visual sensitivity.
• 6:24
  SPEAKER_00: An improvement would suggest that the patient detects dimmer test lights than at baseline.
• 6:28
  SPEAKER_00: However, mean deviation is not a perfect measurement of retinal ganglion cell health.
• 6:33
  SPEAKER_00: It is influenced by patient attention, fatigue, learning effects, cataract or ocular surface disease, refractive correction, test reliability, day-to-day biological variability.
• 6:45
  SPEAKER_00: A single positive mean deviation result would therefore be insufficient to prove neural recovery.
• 6:51
  SPEAKER_00: Secondary visual field assessments.
• 6:53
  SPEAKER_00: Visual field mean deviation is also measured at day 28, day 84, day 252, day 336.
• 7:01
  SPEAKER_00: The later measurements are particularly valuable because the treatment period ends at approximately day 168.
• 7:08
  SPEAKER_00: If a benefit remains at days 252 and 336, that would support a persistent biological effect rather than a short-lived testing artifact.
• 7:17
  SPEAKER_00: The trial does not appear to use a conventional long-term visual field slope as its primary endpoint.
• 7:23
  SPEAKER_00: That is a limitation.
• 7:25
  SPEAKER_00: A 24-week period is short for proving that glaucoma progression has slowed, particularly when visual field tests are noisy.
• 7:33
  SPEAKER_00: Retinal nerve fiber layer thickness.
• 7:36
  SPEAKER_00: The trial measures retinal nerve fiber layer thickness by optical coherence tomography at days 28, 84, 168, 252, and 336.
• 7:46
  SPEAKER_00: The retinal nerve fiber layer contains the axons of retinal ganglion cells as they converge toward the optic nerve.
• 7:52
  SPEAKER_00: A successful neuroprotective drug might cause slower thinning, stabilization of thickness, or, less likely, measurable thickening if some axons or supporting structures recover.
• 8:05
  SPEAKER_00: A major caution is that dead retinal ganglion cell axons cannot normally be restored simply by keeping the remaining cells healthy.
• 8:13
  SPEAKER_00: Therefore, the most realistic structural result would be less thinning, not a large increase in retinal nerve fiber layer thickness.
• 8:20
  SPEAKER_00: Macular ganglion cell inner plexiform layer.
• 8:23
  SPEAKER_00: The trial also measures the macular ganglion cell inner plexiform layer.
• 8:27
  SPEAKER_00: This layer is often useful because it captures the cell bodies and dendritic structures of retinal ganglion cells in the central retina.
• 8:35
  SPEAKER_00: It may be more sensitive than peripapillary retinal nerve fiber layer measurements in some stages of glaucoma.
• 8:42
  SPEAKER_00: Again, an apparent increase could have several explanations.
• 8:46
  SPEAKER_00: Genuine recovery of stressed cells, changes in dendritic structure, altered tissue hydration, segmentation error, measurement noise.
• 8:55
  SPEAKER_00: A convincing result would require reproducible, dose-related preservation across multiple scans and preferably agreement with visual field and visual evoked potential findings.
• 9:06
  SPEAKER_00: Pattern visual evoked potential.
• 9:08
  SPEAKER_00: The trial measures the P100 wave amplitude and latency of the pattern visual evoked potential.
• 9:14
  SPEAKER_00: This test records electrical responses from the visual system after a patterned image is shown.
• 9:20
  SPEAKER_00: In general, higher P100 amplitude can indicate stronger visual pathway responses.
• 9:26
  SPEAKER_00: Shorter P100 latency can indicate faster conduction.
• 9:30
  SPEAKER_00: The test is potentially valuable because it examines function along the visual pathway rather than only the retina.
• 9:36
  SPEAKER_00: However, it is affected by visual acuity, attention, refractive error, electrode placement, and technical factors.
• 9:44
  SPEAKER_00: A genuine recovery signal would ideally involve improved or preserved mean deviation, increased or stabilized P100 amplitude, reduced or stabilized P100 latency, no meaningful intraocular pressure difference between treatment groups.
• 10:00
  SPEAKER_00: Pharmacokinetics and immunogenicity.
• 10:02
  SPEAKER_00: The study also plans to measure drug concentrations in tears, drug concentrations in plasma, anti-drug antibodies, neutralizing antibodies.
• 10:11
  SPEAKER_00: This is important because recombinant proteins can be cleared rapidly from the ocular surface and can sometimes provoke immune responses.
• 10:19
  SPEAKER_00: But tear and plasma measurements do not directly prove that the drug reaches retinal ganglion cells or optic nerve axons.
• 10:26
  SPEAKER_00: Safety monitoring.
• 10:27
  SPEAKER_00: Safety assessments include adverse events, ocular symptoms, slit lamp and ophthalmic examinations, visual acuity, intraocular pressure, physical examinations, vital signs, laboratory testing, 12-led electrocardiograms, immunogenicity testing.
• 10:44
  SPEAKER_00: Safety monitoring continues through the post-study period, approximately 48 weeks after the first dose.
• 10:49
  SPEAKER_00: G01 trial record.
• 10:51
  SPEAKER_00: What exactly is RHNGFV2?
• 10:53
  SPEAKER_00: The likely mutation.
• 10:55
  SPEAKER_00: The public evidence strongly links RNGF V2 to a K34D mutation in mature human nerve growth factor.
• 11:02
  SPEAKER_00: In plain language, the molecule replaces K lysine, a positively charged amino acid, with D aspartate, a negatively charged amino acid, at position 34 of mature nerve growth factor.
• 11:13
  SPEAKER_00: The relevant sequence region changes from approximately.
• 11:16
  SPEAKER_00: The patent family assigned to Human Cell Co.
• 11:19
  SPEAKER_00: identifies RHNGF V2 as NGF carity4D and states that it differs from wild type human nerve growth factor by one amino acid.
• 11:27
  SPEAKER_00: Human Cell Co.
• 11:28
  SPEAKER_00: NGF variant patent RHNGF V2 antibody patent description.
• 11:33
  SPEAKER_00: Important qualification.
• 11:35
  SPEAKER_00: The clinical registry does not publish a full analytical certificate for the G01 clinical batches.
• 11:40
  SPEAKER_00: The company identifies Erosethro I as containing RHNGF V2, and the patent describes RHNGF V2 as K34D, but an independent laboratory confirmation of the exact clinical product is not publicly available.
• 11:54
  SPEAKER_00: Therefore, established evidence G01 contains the developer's proprietary or HNGF V2.
• 12:00
  SPEAKER_00: Strong inference, RHNGF V2 is the K34D variant described in the Human Cell Co-patent.
• 12:07
  SPEAKER_00: Not independently verified, the complete formulation, excipients, aggregation profile, final three-dimensional structure, and clinical batch release specifications.
• 12:16
  SPEAKER_00: Why make this mutation?
• 12:18
  SPEAKER_00: Nerve growth factor signals through two important receptor systems, THRKA, which generally supports neuronal survival, growth, and repair.
• 12:26
  SPEAKER_00: P75 neurotrophin receptor, which can support survival in some settings, but can also participate in pain, inflammation, axonal collapse, and cell death, particularly when activated by pro-nerve growth factor or when Tarkea signaling is impaired.
• 12:42
  SPEAKER_00: The patent reports that K34D retained strong activity at Tarkea, had approximately twice the activity of wild type nerve growth factor in a cell proliferation assay, reduced binding to the P75 neurotrophin receptor by approximately 27-fold, increased the apparent Tarkea to P75 selectivity ratio from approximately 9.4 for wild type nerve growth factor to approximately 72 for K34D.
• 13:08
  SPEAKER_00: The reported TERKAA cell proliferation half maximal effective concentration was.
• 13:13
  SPEAKER_00: For the full table, please open this article on visualfieldtest.com.
• 13:17
  SPEAKER_00: These are laboratory receptor and cell assay findings, not human glaucoma outcomes.
• 13:22
  SPEAKER_00: Human Cell Co NGF variant patent.
• 13:24
  SPEAKER_00: Does K34D eliminate nerve growth factor pain?
• 13:28
  SPEAKER_00: Not necessarily.
• 13:29
  SPEAKER_00: The patent suggests that some related variants, especially the double mutant K34D-K32D, may produce less persistent pain in a rat pain model.
• 13:38
  SPEAKER_00: However, K34D alone did not clearly eliminate pain in that model.
• 13:43
  SPEAKER_00: This matters because conventional topical recombinant human nerve growth factor has been associated with periocular discomfort and eye pain.
• 13:51
  SPEAKER_00: The earlier glaucoma phase 1B trial found periocular ache in 52% of RHNGF treated participants compared with 5% of placebo-treated participants.
• 14:01
  SPEAKER_00: Human Cell Co.
• 14:02
  SPEAKER_00: NGF variant patent phase 1B glaucoma trial.
• 14:06
  SPEAKER_00: Why nerve growth factor could help in glaucoma?
• 14:09
  SPEAKER_00: Glaucoma is not simply an eye pressure disorder.
• 14:12
  SPEAKER_00: It is a neurodegenerative disease involving mechanical stress at the optic nerve head, impaired axonal transport, mitochondrial stress, oxidative injury, abnormal calcium signaling, inflammation, altered glial activity, retinal ganglion cell dysfunction, and eventual program cell death.
• 14:29
  SPEAKER_00: Elevated intraocular pressure can disrupt the movement of survival signals from the brain and optic nerve targets back to retinal ganglion cells.
• 14:38
  SPEAKER_00: The result resembles a form of neurotrophic deprivation.
• 14:41
  SPEAKER_00: Nerve growth factor could theoretically compensate by activating survival signaling directly in retinal ganglion cells.
• 14:48
  SPEAKER_00: Tier Ka activation can stimulate pathways involving phosphoonocidide III kinase and protein kinase B, mitogen-activated protein kinase, and extracellular signal-regulated kinase, antiapoptotic proteins such as B cell lymphoma 2, axonal transport, and cytoskeletal maintenance, neuronal plasticity and synaptic support.
• 15:09
  SPEAKER_00: Reviews of glaucoma neuroprotection identify nerve growth factor, brain-derived neurotrophic factor, and ciliary neurotrophic factor as possible ways to support retinal ganglion cell survival.
• 15:21
  SPEAKER_00: However, they also emphasize that neurotrophic factor delivery and receptor balance remain major obstacles.
• 15:28
  SPEAKER_00: Neuroprotection in glaucoma review.
• 15:31
  SPEAKER_00: Neuroprotection in glaucoma, mechanisms beyond intraocular pressure lowering, animal evidence behind the G01 program.
• 15:39
  SPEAKER_00: The original topical nerve growth factor glaucoma study.
• 15:42
  SPEAKER_00: In a rat model of chronic ocular hypertension, researchers applied murine nerve growth factor eye drops at 200 micrograms milliliter four times daily for seven weeks.
• 15:53
  SPEAKER_00: The untreated glaucomatous eyes lost approximately 40% of their retinal ganglion cells.
• 15:58
  SPEAKER_00: The reported retinal ganglion cell densities were approximately normal control eyes, 3,155 cells per square millimeter, untreated glaucomatous eyes, 1,850 cells per square millimeter, nerve growth factor treated glaucomatous eyes, 2,530 cells per square millimeter.
• 16:18
  SPEAKER_00: Using these values, treatment reduced the estimated number of lost cells by approximately half compared with untreated glaucoma.
• 16:25
  SPEAKER_00: The treatment was associated with fewer terminal deoxynucleotid transferase DUTP, NICN labeling positive apoptotic cells, lower expression of the proepoptoin BACs, higher expression of the survival protein, B cell lymphoma 2, a more favorable B cell lymphoma 2 to BACs ratio.
• 16:44
  SPEAKER_00: This is strong evidence that conventional nerve growth factor can prevent retinal ganglion cell death in at least one animal model.
• 16:52
  SPEAKER_00: It does not prove that the same effect occurs in people.
• 16:56
  SPEAKER_00: Lambies and colleagues, proceedings of the National Academy of Sciences PubMed record, optic nerve injury studies.
• 17:03
  SPEAKER_00: In a rat optic nerve crush model, both intravitrial and topical recombinant human nerve growth factor reduced retinal ganglion cell loss and stimulated some axonal regrowth.
• 17:14
  SPEAKER_00: The reported biological changes included increased phosphorylation of TKA, reduced P75 neurotrophin receptor and pro-nerve growth factor, reduced NOGO A and Rho associated protein kinase II signaling, reduced markers associated with glial scarring, improvement in retinal and optic nerve injury responses.
• 17:34
  SPEAKER_00: This study is relevant because it suggests that nerve growth factor may do more than keep cell bodies alive.
• 17:40
  SPEAKER_00: It might also affect the injured axon environment.
• 17:43
  SPEAKER_00: However, optic nerve crush is an acute injury model.
• 17:47
  SPEAKER_00: Chronic glaucoma is slower, more complex, and involves years of mechanical and metabolic stress.
• 17:53
  SPEAKER_00: Nerve growth factor in optic nerve injury.
• 17:56
  SPEAKER_00: The K34D patent model, the Human Cell Co.
• 18:00
  SPEAKER_00: patent describes a chronic ratocular hypertension model using episcleral vein cauterization.
• 18:06
  SPEAKER_00: Important findings included intraocular pressure increased to approximately 20 to 32 mm of mercury.
• 18:12
  SPEAKER_00: Treatment began after glaucoma had already been induced.
• 18:16
  SPEAKER_00: Treatment did not lower intraocular pressure.
• 18:19
  SPEAKER_00: K34D at 200 micrograms per milliliter protected retinal ganglion cells and optic nerve axons.
• 18:25
  SPEAKER_00: Wild type nerve growth factor at the same concentration was not effective in that model.
• 18:30
  SPEAKER_00: Pattern electroretinogram amplitude was approximately 20% higher than placebo after 20 weeks with K34D or K34D K32D.
• 18:40
  SPEAKER_00: In another experiment, reported retinal ganglion cell loss was For the full table, please open this article on VisualFieldTest.com.
• 18:48
  SPEAKER_00: That represents roughly a 50% relative reduction in cell loss compared with vehicle.
• 18:54
  SPEAKER_00: These results are encouraging, especially because the drug did not work by lowering pressure.
• 18:59
  SPEAKER_00: But they come from a company patent, small animal groups, and experiments that have not yet been independently replicated in a peer-reviewed clinical paper.
• 19:08
  SPEAKER_00: They should be viewed as supportive preclinical evidence, not proof of clinical effectiveness.
• 19:14
  SPEAKER_00: Human Cell Co NGF variant patent.
• 19:18
  SPEAKER_00: Human evidence before G01, 3-patient glaucoma case series.
• 19:23
  SPEAKER_00: The earliest human glaucoma experience involved three patients with advanced progressive glaucoma, despite apparently controlled intraocular pressure.
• 19:32
  SPEAKER_00: They received topical murine nerve growth factor at 200 micrograms milliliter four times daily for three months.
• 19:39
  SPEAKER_00: Reported findings included visual field improvement in two patients, visual field stabilization in one patient, improved pattern electroretinogram responses, improved visual evoked potential responses, better contrast sensitivity, improvement in visual acuity, persistence of some effects after treatment stopped.
• 19:59
  SPEAKER_00: Two patients reportedly remained improved during longer follow-up.
• 20:03
  SPEAKER_00: This is the most direct human evidence suggesting that nerve growth factor might improve function in living but severely stressed retinal ganglion cells.
• 20:13
  SPEAKER_00: Unfortunately, it is also one of the weakest forms of clinical evidence because there were only three patients.
• 20:19
  SPEAKER_00: There was no placebo group, there was no randomization, the treatment used murine nerve growth factor, not G01, patients were selected for compassionate treatment.
• 20:30
  SPEAKER_00: Repeated visual field testing can produce learning and variability effects.
• 20:35
  SPEAKER_00: The study is best interpreted as hypothesis generating.
• 20:39
  SPEAKER_00: Lambiase and colleagues, proceedings of the National Academy of Sciences.
• 20:43
  SPEAKER_00: The randomized Phase 1B trial, a later randomized, double-masked, vehicle-controlled phase 1B trial, evaluated conventional recombinant human nerve growth factor in 60 patients with open-angle glaucoma.
• 20:57
  SPEAKER_00: Participants received recombinant human nerve growth factor at 180 micrograms milliliter, one drop in both eyes three times daily, treatment for eight weeks, follow-up for an additional 24 weeks.
• 21:09
  SPEAKER_00: The trial found no treatment-related serious adverse events, no meaningful intraocular pressure safety signal, no drug-related systemic toxicity, periocular ache in 52% of treated participants versus 5% of placebo participants, treatment discontinuation because of discomfort in 7.5% of treated participants, no statistically significant difference in global visual field indices, no statistically significant difference in retinal nerve fiber layer thickness.
• 21:39
  SPEAKER_00: The authors reported non significant trends favoring recombinant human nerve growth factor, but the trial did not establish short term neuroenhancement.
• 21:48
  SPEAKER_00: It did, however, support the feasibility of moving toward a longer neuroprotection study.
• 21:53
  SPEAKER_00: Phase 1B randomized glaucoma trial, PubMed.
• 21:57
  SPEAKER_00: What does the phase a B trial mean for G01?
• 22:00
  SPEAKER_00: It creates both reassurance and caution.
• 22:02
  SPEAKER_00: Reassurance.
• 22:03
  SPEAKER_00: Topical recombinant human nerve growth factor can be administered to glaucoma patients.
• 22:08
  SPEAKER_00: Serious toxicity was not observed.
• 22:11
  SPEAKER_00: The drug did not appear to raise intraocular pressure.
• 22:14
  SPEAKER_00: Some structural and functional trends favored treatment.
• 22:17
  SPEAKER_00: Caution.
• 22:18
  SPEAKER_00: The trial was small.
• 22:19
  SPEAKER_00: Treatment lasted only eight weeks.
• 22:21
  SPEAKER_00: The molecule was not RHNGF V2.
• 22:24
  SPEAKER_00: The study was not designed to detect long-term slowing of glaucoma progression.
• 22:29
  SPEAKER_00: The functional results were not statistically significant.
• 22:32
  SPEAKER_00: GO1 is therefore not starting from zero, but it also is not entering phase 2 with established human efficacy.
• 22:39
  SPEAKER_00: Can an eyedrop reach the retina and optic nerve?
• 22:43
  SPEAKER_00: This is the most important scientific uncertainty.
• 22:46
  SPEAKER_00: Why delivery is difficult, the drug is a relatively large protein.
• 22:50
  SPEAKER_00: After an eyedrop is placed on the surface, most of the dose is lost through blinking, tear drainage, dilution by the tear film, binding to the ocular surface, enzymatic breakdown, absorption into the conjunctiva and nasal tissues, systemic clearance.
• 23:05
  SPEAKER_00: The cornea and sclera also limit movement toward the posterior eye.
• 23:10
  SPEAKER_00: Earlier animal evidence.
• 23:12
  SPEAKER_00: Earlier animal studies detected topical nerve growth factor in the retina and optic nerve and found biological effects there.
• 23:18
  SPEAKER_00: This supports the idea that some drug can cross ocular barriers through conjunctival, scleral, uveal, or possibly periotic pathways, but detectable does not necessarily mean therapeutically sufficient.
• 23:32
  SPEAKER_00: Newer quantitative pharmacokinetic evidence.
• 23:34
  SPEAKER_00: A 2025 stable isotope study used labeled recombinant human nerve growth factor to measure exactly where the protein went after topical dosing in rats and rabbits.
• 23:44
  SPEAKER_00: The findings were sobering.
• 23:46
  SPEAKER_00: Topical eye drops produced less than 0.04% of the instilled dose in the retina.
• 23:52
  SPEAKER_00: After repeated topical dosing, reported retinal exposure was approximately 0.003% to 0.06% of the delivered dose.
• 24:01
  SPEAKER_00: Intravitrial injection produced approximately 1.8% to 4.0% of the dose in the retina.
• 24:08
  SPEAKER_00: Intravitrial delivery also produced sustained exposure in the retina and optic nerve for up to 60 days.
• 24:14
  SPEAKER_00: This does not prove that eye drops cannot work.
• 24:18
  SPEAKER_00: Nerve growth factor receptors bind their ligand with high affinity, and a small amount may be biologically active.
• 24:24
  SPEAKER_00: But it strongly suggests that topical dosing is an inefficient way to deliver a large protein to the posterior segment.
• 24:31
  SPEAKER_00: Human nerve growth factor delivery to the retina.
• 24:34
  SPEAKER_00: Full study, G01 dose compared with earlier recombinant human nerve growth factor, A33 microliter drop contains approximately 3.3 micrograms at 100 micrograms milliliter, 6.6 micrograms at 200 micrograms milliliter.
• 24:51
  SPEAKER_00: At twice daily dosing, the high G01 dose delivers approximately 13.2 micrograms per eye per day.
• 24:58
  SPEAKER_00: The earlier phase 1B trial used approximately 35 microliters of 180 micrograms milliliter three times daily, approximately 6.3 micrograms per drop, approximately 18.9 micrograms per eye per day.
• 25:13
  SPEAKER_00: Thus, the high G01 dose provides roughly 30% less total daily protein than the earlier 180 micrograms milliliter regimen, although G01 may be more potent at its target receptors.
• 25:25
  SPEAKER_00: Tear pharmacokinetics are not retinal pharmacokinetics.
• 25:29
  SPEAKER_00: A separate 2025 study of another recombinant human nerve growth factor product found tear fluid peak concentration at approximately 0.17 hours, tear fluid half-life of approximately 4.21 hours, no detectable drug or antidrug antibodies in peripheral blood.
• 25:46
  SPEAKER_00: This demonstrates local ocular surface exposure, but does not prove that the drug reaches retinal ganglion cells.
• 25:53
  SPEAKER_00: Recombinant human nerve growth factor pharmacokinetics in healthy subjects.
• 25:58
  SPEAKER_00: My assessment of penetration established evidence, topical nerve growth factor can reach posterior ocular tissues in some animal experiments.
• 26:07
  SPEAKER_00: Strong inference, only a very small fraction of the dose reaches the human retina after topical application.
• 26:14
  SPEAKER_00: Plausible speculation.
• 26:16
  SPEAKER_00: RHNGFE2 might still reach enough Tarka receptors to produce a biological effect because the receptor is high affinity and the molecule may be more potent than wild-type nerve growth factor.
• 26:27
  SPEAKER_00: The G01 phase II trial measures tear and plasma concentrations, but not retinal or optic nerve tissue concentrations.
• 26:36
  SPEAKER_00: Therefore, even a negative trial would not fully distinguish the molecule does not work from the molecule did not reach the target.
• 26:44
  SPEAKER_00: What could NGF actually do?
• 26:47
  SPEAKER_00: 8.1 Prevent retinal ganglion cell death.
• 26:50
  SPEAKER_00: This is the strongest mechanistic claim.
• 26:53
  SPEAKER_00: Animal glaucoma and optic nerve injury studies consistently support improved retinal ganglion cell survival after nerve growth factor treatment.
• 27:01
  SPEAKER_00: The K34D patent also reports preservation of retinal ganglion cells and axons without lowering intraocular pressure.
• 27:08
  SPEAKER_00: Classification established in animals, not yet established in humans.
• 27:12
  SPEAKER_00: 8.2 Restore function in stressed but living retinal ganglion cells.
• 27:17
  SPEAKER_00: This is biologically plausible.
• 27:20
  SPEAKER_00: A retinal ganglion cell can be fully functional, metabolically stressed but still alive, alive but electrically dysfunctional, disconnected or unable to transport signals normally, irreversibly dead.
• 27:32
  SPEAKER_00: Nerve growth factor could potentially help cells in the middle categories by improving mitochondrial survival signaling, restoring axonal transport, reducing apoptotic pressure, improving dendritic or synaptic function, shifting signaling away from P75 mediated stress pathways, increasing the ability of the cell to respond to visual input.
• 27:53
  SPEAKER_00: The human three-patient case series and some animal pattern electroretinogram findings support this possibility.
• 28:00
  SPEAKER_00: The randomized phase 1B study did not prove it.
• 28:03
  SPEAKER_00: Classification: strong biological inference with limited human support.
• 28:08
  SPEAKER_00: 8.3 regenerate optic nerve axons.
• 28:11
  SPEAKER_00: This is much less certain.
• 28:12
  SPEAKER_00: In an optic nerve crush model, topical and intravitreal recombinant human nerve growth factor were associated with some axonal regrowth, but there is a large difference between stimulating short-distance axonal sprouting, restoring local axonal transport, reconnecting an injured axon to the correct brain target, restoring a useful visual map.
• 28:33
  SPEAKER_00: Glaucoma is a chronic disease.
• 28:35
  SPEAKER_00: Many axons are lost gradually over years, and the optic nerve contains long projections to the brain.
• 28:41
  SPEAKER_00: A topical nerve growth factor molecule alone is unlikely to rebuild the entire visual pathway once axons have disappeared.
• 28:49
  SPEAKER_00: Classification.
• 28:50
  SPEAKER_00: Plausible in selected injury settings, speculative as a clinically meaningful glaucoma regeneration treatment.
• 28:57
  SPEAKER_00: Could visual field mean deviation improve?
• 29:00
  SPEAKER_00: Yes, but the result would require unusually strong evidence, or a visual field mean deviation score can improve for reasons unrelated to retinal ganglion cell recovery, patient learning, better concentration, improved refractive correction, cataract surgery, ocular surface improvement, less fatigue, random test-retest variation, regression toward the mean.
• 29:22
  SPEAKER_00: A true neural improvement is more credible if it is present on at least two or three repeated fields, dose-related, larger than expected test-retest variability, accompanied by improved pattern visual-evoked potential responses, accompanied by stabilization or improvement in ganglion cell measurements, still present after treatment stops, independent of intraocular pressure differences.
• 29:46
  SPEAKER_00: What size of improvement would matter?
• 29:49
  SPEAKER_00: A small placebo-adjusted improvement of 0.2 or 0.3 decibels would be difficult to interpret.
• 29:56
  SPEAKER_00: A more compelling phase two signal would be approximately 1 decibel or more of placebo-adjusted improvement confirmed on repeated tests present in both active dose groups or showing a clear dose response, supported by visual evoke potential results, without evidence of a testing or masking artifact.
• 30:14
  SPEAKER_00: Even that would not prove that dead retinal ganglion cells had been replaced.
• 30:19
  SPEAKER_00: It would more likely indicate that surviving but dysfunctional cells had become more responsive.
• 30:26
  SPEAKER_00: Could a severely damaged patient improve?
• 30:29
  SPEAKER_00: Possibly, but the trial does not directly answer this question because it excludes many patients with end-stage disease.
• 30:36
  SPEAKER_00: The best candidates would probably be patients with measurable remaining visual field, residual retinal ganglion cells, ongoing functional decline, relatively preserved central vision, good intraocular pressure control, no major competing retinal or optic nerve disease.
• 30:55
  SPEAKER_00: A patient with only a tiny central island of vision may have fewer viable cells capable of recovery and more floor effects in both visual field and optical coherence tomography measurements.
• 31:05
  SPEAKER_00: The prior three-patient case series included advanced glaucoma, but that evidence is too weak to establish benefit.
• 31:12
  SPEAKER_00: Does GO1 need excellent intraocular pressure control?
• 31:16
  SPEAKER_00: Almost certainly.
• 31:17
  SPEAKER_00: GO1 does not appear to lower intraocular pressure.
• 31:20
  SPEAKER_00: The K34D animal studies specifically reported neuroprotection without a pressure-lowering effect.
• 31:27
  SPEAKER_00: The most sensible use of GO1 would be add on therapy.
• 31:30
  SPEAKER_00: Surgery or pressure-lowering drops reduce the damaging mechanical stress.
• 31:35
  SPEAKER_00: GO1 supports the survival and function of retinal ganglion cells.
• 31:39
  SPEAKER_00: The two approaches act on different parts of the disease process.
• 31:43
  SPEAKER_00: If pressure remains high or fluctuates substantially, continued mechanical injury could overwhelm the drug's survival signal.
• 31:50
  SPEAKER_00: The current trial requires pressure between 10 and 21 mm of mercury and considers it stable.
• 31:57
  SPEAKER_00: That is an appropriate design for testing and effect independent of pressure reduction.
• 32:02
  SPEAKER_00: However, the trial should report mean pressure throughout treatment, peak and fluctuation measurements where available, medication changes, prior laser or surgery, pressure differences between treatment arms.
• 32:16
  SPEAKER_00: A positive visual field result with no intraocular pressure difference would be especially important.
• 32:22
  SPEAKER_00: Could GO1 combine with other therapies?
• 32:26
  SPEAKER_00: Trabeculectomy and other pressure-lowering surgery.
• 32:29
  SPEAKER_00: Mechanistically complementary.
• 32:31
  SPEAKER_00: Surgery reduces the initiating mechanical stress.
• 32:34
  SPEAKER_00: G01 could theoretically protect surviving retinal ganglion cells during and after pressure control.
• 32:41
  SPEAKER_00: However, the current trial excludes recent filtering surgery and planned surgery.
• 32:46
  SPEAKER_00: It therefore will not establish the safety or efficacy of immediate postoperative combination treatment.
• 32:52
  SPEAKER_00: Prostaglandin analogues.
• 32:54
  SPEAKER_00: Likely compatible but not proven synergistic.
• 32:57
  SPEAKER_00: Prostaglandin analogues lower intraocular pressure through increased aqueous outflow.
• 33:02
  SPEAKER_00: They do not directly replace a trophic survival signal.
• 33:06
  SPEAKER_00: A future trial could compare.
• 33:08
  SPEAKER_00: Pressure lowering treatment alone, pressure lowering treatment plus GO1, GO1 alone would be ethically less appropriate in patients who need pressure control.
• 33:17
  SPEAKER_00: Rhoe associated protein kinase inhibitors.
• 33:21
  SPEAKER_00: This is an interesting theoretical combination.
• 33:23
  SPEAKER_00: Rho associated protein kinase signaling is involved in axonal collapse, cytoskeletal stress, optic nerve injury, aqueous outflow resistance.
• 33:33
  SPEAKER_00: The optic nerve crush study reported normalization of row associated protein kinase II-related signaling after topical nerve growth factor.
• 33:41
  SPEAKER_00: A row associated protein kinase inhibitor could therefore potentially complement the K34D strategy.
• 33:48
  SPEAKER_00: But this is a mechanistic hypothesis, not a demonstrated clinical synergy.
• 33:53
  SPEAKER_00: Nicotinamide.
• 33:54
  SPEAKER_00: Nicotinamide supports nicotinamide adenine dinucleotide metabolism and mitochondrial energy production.
• 34:00
  SPEAKER_00: It addresses a different vulnerability from nerve growth factor.
• 34:04
  SPEAKER_00: Nicotinamide, metabolic resilience, G1, trophic and antiapoptotic signaling.
• 34:10
  SPEAKER_00: A combination could be biologically attractive.
• 34:13
  SPEAKER_00: However, the G01 phase II protocol excludes nicotinamide, so the trial will not answer this question.
• 34:19
  SPEAKER_00: Gene therapy.
• 34:20
  SPEAKER_00: A gene therapy could provide prolonged expression of a neuroprotective factor, while G01 could provide a temporary or adjustable treatment.
• 34:29
  SPEAKER_00: Potential advantages of combination treatment include broader pathway coverage, lower dose of each agent, treatment during the period before gene expression becomes established.
• 34:39
  SPEAKER_00: Potential risks include excessive trophic signaling, inflammation, immune reactions, altered receptor sensitivity, difficulty reversing treatment.
• 34:50
  SPEAKER_00: No clinical evidence currently establishes that G01 can be safely combined with optic nerve gene therapy, comparison with other neuroprotective approaches.
• 34:59
  SPEAKER_00: For the full table, please open this article on visualfieldtest.com.
• 35:03
  SPEAKER_00: ASP2767.
• 35:06
  SPEAKER_00: ASP2767 is not an eyedrop.
• 35:08
  SPEAKER_00: It is an ocular gene therapy program involving a single intravitreal injection with phase 1 dose escalation and a planned randomized phase 2 component.
• 35:18
  SPEAKER_00: The public protocol includes patients with moderate to advanced glaucoma, serial visual field testing, optical coherence tomography measurements, and approximately one year of follow-up.
• 35:29
  SPEAKER_00: Its advantage is that intravitreal delivery is much more efficient for reaching the retina than a topical protein drop.
• 35:36
  SPEAKER_00: Its disadvantages are the risks associated with an invasive gene therapy procedure, inflammation, immune responses, and a treatment that is difficult to remove once administered.
• 35:46
  SPEAKER_00: ASP 2767 trial record, ER100-ER100, belongs to a more ambitious category.
• 35:54
  SPEAKER_00: Gene-based cellular reprogramming intended to restore a more youthful or resilient state in damaged retinal ganglion cells.
• 36:02
  SPEAKER_00: Compared with G01, it is not a replacement protein.
• 36:06
  SPEAKER_00: It is not easily stopped once administered.
• 36:08
  SPEAKER_00: Its mechanism is broader and potentially more powerful.
• 36:12
  SPEAKER_00: It carries greater uncertainty about long-term cellular effects.
• 36:16
  SPEAKER_00: There is no established human efficacy evidence for glaucoma as of September 4, 2026.
• 36:22
  SPEAKER_00: GO1 is more conservative.
• 36:24
  SPEAKER_00: It provides a transient, adjustable signal and can theoretically be discontinued immediately.
• 36:29
  SPEAKER_00: NT501 and ciliary neurotrophic factor NT501 is an encapsulated cell implant designed to release ciliary neurotrophic factor inside the eye over an extended period.
• 36:41
  SPEAKER_00: It offers a more reliable posterior segment delivery method than an eye drop, but requires surgery.
• 36:47
  SPEAKER_00: The major lesson from NT501 is that neurotrophic factors may need sustained intraocular exposure.
• 36:54
  SPEAKER_00: However, ciliary neurotrophic factor can also produce retinal remodeling, and the optimal dose may not be straightforward.
• 37:01
  SPEAKER_00: Glaucoma-specific efficacy remains investigational.
• 37:04
  SPEAKER_00: Phase 1 NT501 glaucoma trial, neuroprotection review.
• 37:08
  SPEAKER_00: Nicotinamide nicotinamide is not a growth factor.
• 37:12
  SPEAKER_00: Its rationale is that retinal ganglion cells become metabolically vulnerable when energy production and nicotinamide-addenine dinucleotide reserves are inadequate.
• 37:22
  SPEAKER_00: Animal studies are encouraging and early human research is ongoing.
• 37:26
  SPEAKER_00: It may eventually prove useful in combination with a trophic treatment such as GRO1, but that combination has not been tested.
• 37:34
  SPEAKER_00: Bramonidine, bromonidine has potential neuroprotective effects in laboratory models and may increase brain-derived neurotrophic factor expression.
• 37:43
  SPEAKER_00: The low-pressure glaucoma treatment study suggested less visual field progression with bromonidine than Timolol, but interpretation was complicated by high dropout and the possibility that the comparison drug affected outcomes.
• 37:56
  SPEAKER_00: A Cochrane review concluded that the evidence was too uncertain to establish independent neuroprotection.
• 38:03
  SPEAKER_00: Cochrane Review of Glaucoma Neuroprotection.
• 38:06
  SPEAKER_00: Bramonidine Neuroprotection Review.
• 38:09
  SPEAKER_00: Citycaline-Cydycline has produced encouraging findings in some small studies involving pattern electroretinograms, visual-evoked potentials, and visual field measures.
• 38:19
  SPEAKER_00: But a 2023 systematic review involving 10 studies and 424 patients found no significant overall difference in intraocular pressure, mean deviation, retinal nerve fiber layer thickness, or pattern electroetinogram amplitude between cytochaline and control groups.
• 38:37
  SPEAKER_00: That makes cytocholine biologically interesting, but clinically unproven.
• 38:42
  SPEAKER_00: Cytocholine Systematic Review, brain-derived neurotrophic factor.
• 38:46
  SPEAKER_00: Brain-derived neurotrophic factor acts mainly through the TART-KB receptor.
• 38:50
  SPEAKER_00: In animal glaucoma models, viral brain-derived neurotrophic factor expression has increased retinal ganglion cell survival.
• 38:58
  SPEAKER_00: The main problems are delivery, short biological duration, receptor downregulation, and the inability of a growth factor alone to reconnect dead axons.
• 39:08
  SPEAKER_00: G01 has a potential advantage over brain-derived neurotrophic factor because the K34D molecule is designed to favor TKA signaling and reduce P75 related effects.
• 39:20
  SPEAKER_00: Evidence classification.
• 39:22
  SPEAKER_00: Established evidence, lowering intraocular pressure remains the only clearly established treatment for slowing glaucoma progression.
• 39:30
  SPEAKER_00: Nerv growth factor can activate neuronal survival pathways.
• 39:33
  SPEAKER_00: Topical nerve growth factor protects retinal ganglion cells in several animal models.
• 39:38
  SPEAKER_00: Conventional recombinant human nerve growth factor is clinically usable as an eye drop.
• 39:43
  SPEAKER_00: Senigermin, a recombinant human nerve growth factor product, is effective for neurotrophic keratitis by healing the cornea and supporting corneal nerves.
• 39:52
  SPEAKER_00: The G01 phase II trial is real, ongoing, randomized, masked, placebo-controlled, and designed to test visual function independently of pressure lowering.
• 40:03
  SPEAKER_00: HNGFV2 is strongly linked to the K34D variant described in the Human Cell Co-patent.
• 40:10
  SPEAKER_00: Strong inference G01 is intended primarily to prevent retinal ganglion cell death and preserve function rather than regenerate large numbers of lost neurons.
• 40:19
  SPEAKER_00: K34D was designed to retain TRKA activity while reducing P75 neurotrophin receptor signaling.
• 40:26
  SPEAKER_00: Any benefit will probably be greatest in patients with stressed but still living retinal ganglion cells.
• 40:33
  SPEAKER_00: Excellent intraocular pressure control will probably remain necessary.
• 40:38
  SPEAKER_00: A positive visual field result would be more convincing if it were accompanied by visual-evoked potential improvement and structural stabilization.
• 40:46
  SPEAKER_00: Topical penetration is probably low, but may not be zero.
• 40:50
  SPEAKER_00: Plausible speculation G01 could restore measurable function in some damaged retinal ganglion cells.
• 40:57
  SPEAKER_00: A meaningful subset of patients with moderate or even advanced glaucoma could improve.
• 41:02
  SPEAKER_00: G01 could work synergistically with pressure-lowering surgery, nicotinamide, roe-associated protein kinase inhibition, or gene therapy.
• 41:11
  SPEAKER_00: The K34 D mutation could provide better efficacy or tolerability than conventional recombinant human nerve growth factor.
• 41:19
  SPEAKER_00: A topical treatment could produce a lasting biological effect after the drug is stopped.
• 41:25
  SPEAKER_00: My probability estimates.
• 41:27
  SPEAKER_00: These are analytical estimates, not clinical trial results.
• 41:30
  SPEAKER_00: For the full table, please open this article on VisualFieldtest.com.
• 41:34
  SPEAKER_00: The largest uncertainty is not whether nerve growth factor can affect retinal ganglion cells in principle.
• 41:40
  SPEAKER_00: It can.
• 41:41
  SPEAKER_00: The uncertainty is whether Giro1 can deliver enough K34D to the human posterior eye repeatedly and safely.
• 41:48
  SPEAKER_00: Could this eyedrop actually improve vision?
• 41:51
  SPEAKER_00: Best case scenario, GRO1 reaches the retina and optic nerve in biologically meaningful amounts.
• 41:57
  SPEAKER_00: K34D activates Tarkea signaling, reduces harmful P75 related signaling, improves exonal transport, and rescues retinal ganglion cells that are dysfunctional but not yet dead.
• 42:10
  SPEAKER_00: The phase 2 trial shows a dose-related visual field improvement, repeated mean deviation improvement of approximately 1 decibel or more, preserved or improved P100 visual evoked potential responses, less retinal nerve fiber and ganglion cell thinning, no intraocular pressure difference between groups, persistence of benefit at days 252 and 336, acceptable ocular comfort, and low immunogenicity.
• 42:36
  SPEAKER_00: That would be a major advance.
• 42:38
  SPEAKER_00: It would show that a topical treatment can produce a clinically meaningful pressure-independent improvement in glaucoma.
• 42:45
  SPEAKER_00: Realistic scenario G01 is safe and produces a modest biological signal.
• 42:50
  SPEAKER_00: Possible findings include less visual field decline rather than clear improvement, improved visual evoke potential amplitude in some patients, stabilization of ganglion cell measurements, no obvious retinal nerve fiber layer thickening, stronger effects in the 200 microgram milliliter group, benefit that is detectable after treatment but not dramatic.
• 43:12
  SPEAKER_00: This would be encouraging but not yet a breakthrough.
• 43:15
  SPEAKER_00: A larger, longer trial would be needed.
• 43:18
  SPEAKER_00: Failure scenario.
• 43:20
  SPEAKER_00: The drug does not achieve adequate posterior exposure.
• 43:23
  SPEAKER_00: The trial finds no meaningful visual field difference, no optical coherence tomography difference, no visual evoke potential improvement, substantial discomfort, or poor adherence, no clear dose response.
• 43:37
  SPEAKER_00: This would not necessarily prove that K34D biology is wrong.
• 43:40
  SPEAKER_00: It could mean that a topical eye drop is not an efficient enough delivery system for this protein.
• 43:46
  SPEAKER_00: What would qualify as a genuine glaucoma breakthrough?
• 43:50
  SPEAKER_00: A convincing breakthrough would require more than a statistically significant mean deviation result.
• 43:56
  SPEAKER_00: The strongest evidence would be a replicated placebo-adjusted visual field benefit, preferably at least approximately 1 decibel in phase 2, and a clearly slower rate of decline in a larger confirmatory trial.
• 44:10
  SPEAKER_00: Repeated visual field confirmation showing that the result is not learning, fatigue, or test variability.
• 44:16
  SPEAKER_00: Concordant visual evoke potential improvement, especially increased P100 amplitude or improved latency.
• 44:24
  SPEAKER_00: Structural preservation, demonstrated by slower retinal nerve fiber layer and ganglion cell interplexiform layer loss, rather than a suspicious short-term thickening, no meaningful intraocular pressure difference between groups.
• 44:38
  SPEAKER_00: Persistence after treatment withdrawal, suggesting a biological effect rather than a temporary measurement artifact.
• 44:45
  SPEAKER_00: Benefit in patients with established progression, not only stable or very early disease.
• 44:51
  SPEAKER_00: Reproducibility across independent trials and populations.
• 44:55
  SPEAKER_00: A favorable safety profile, especially low pain, low ocular inflammation, and minimal immune response.
• 45:02
  SPEAKER_00: If Gizo1 meets those criteria, it would demonstrate something glaucoma therapy has not yet reliably achieved.
• 45:08
  SPEAKER_00: Direct preservation or recovery of retinal ganglion cell function independently of intraocular pressure lowering.
• 45:15
  SPEAKER_00: That is biologically plausible.
• 45:17
  SPEAKER_00: It is not yet clinically proven.
• 45:19
  SPEAKER_00: All links to sources are available in the text version of this article.
• 45:23
  SPEAKER_00: You can find the full article at VisualFieldTest.com.
• 45:27
  SPEAKER_00: Thanks for listening.
• 45:28
  SPEAKER_00: To check your visual field, click the link at the bottom of this article or visit VisualFieldTest.com.