CG-P5 Peptide for Age-Related Macular Degeneration
Recruiting in Palo Alto (17 mi)
+6 other locations
Age: 18+
Sex: Any
Travel: May Be Covered
Time Reimbursement: Varies
Trial Phase: Phase 1
Recruiting
Sponsor: Caregen Co. Ltd.
Must not be taking: Retina-toxic drugs
Disqualifiers: Uncontrolled diabetes, Glaucoma, others
Breakthrough Therapy
Trial Summary
What is the purpose of this trial?This will be a randomized, comparative, parallel, clinical study to assess initial safety and tolerability of CG-P5 peptide eye drops compared to placebo in patients diagnosed with age-related wet macular degeneration
Will I have to stop taking my current medications?
The trial does not specify if you must stop taking your current medications, but you cannot use medications known to be toxic to the eye or systemic anti-VEGF agents. If you have been treated with certain eye therapies recently, you may need to wait before joining the trial.
What data supports the effectiveness of the drug CG-P5 peptide for age-related macular degeneration?
Research on similar treatments, like avacincaptad pegol, a C5 inhibitor, shows effectiveness in treating geographic atrophy related to age-related macular degeneration. Additionally, studies on peptides that inhibit the complement system, like Compstatin, have shown promise in reducing drusen formation, a key feature of macular degeneration.
12345How is the CG-P5 peptide drug different from other treatments for age-related macular degeneration?
The CG-P5 peptide drug is unique because it is designed to inhibit the complement system, which plays a role in the development of age-related macular degeneration (AMD). This approach targets both dry and wet forms of AMD by potentially preventing the underlying immune response that contributes to the disease, unlike other treatments that may focus on symptoms or different pathways.
12678Eligibility Criteria
This trial is for men and women over 50 with wet age-related macular degeneration (wAMD) in one eye. They must have certain levels of vision clarity, a specific thickness in the retina, and active blood vessel growth under the fovea. Women must be non-childbearing or using birth control. Excluded are those with other major eye diseases, recent surgeries, uncontrolled health conditions like diabetes or hypertension, or who've had certain wAMD treatments recently.Inclusion Criteria
The total size of the lesions in your eyes should not be larger than 12 disc areas, which is about 30.48 square millimeters.
You are able to read and sign a paper agreeing to take part in the study.
You can follow the rules of the study.
+10 more
Exclusion Criteria
I haven't had certain eye treatments in the last 4 months.
Any ophthalmic device implantation within the previous 12 months
Patients with a clinically significant abnormal screening hematology, blood chemistry, or urinalysis, unsuitable for study participation in the investigator's opinion
+22 more
Trial Timeline
Screening
Participants are screened for eligibility to participate in the trial
2-4 weeks
1 visit (in-person)
Treatment
Participants receive CG-P5 peptide eye drops or placebo, with assessments at specified intervals
12 weeks
Visits on Day 0, Day 28, Day 56, and Day 84
Follow-up
Participants are monitored for safety and effectiveness after treatment
4 weeks
Participant Groups
The study tests CG-P5 peptide eye drops against a placebo to see if they're safe for people with wAMD. It's randomized: participants don't choose their treatment group. Some will get the real drug; others won't (placebo). A known treatment called Aflibercept [Eylea] is also part of the study for comparison purposes.
3Treatment groups
Experimental Treatment
Active Control
Placebo Group
Group I: CG-P5 peptide eye dropsExperimental Treatment1 Intervention
Group II: Intravitreal injection of Eylea®Active Control1 Intervention
Group III: Placebo Eye dropsPlacebo Group1 Intervention
Find a Clinic Near You
Research Locations NearbySelect from list below to view details:
CBCC Global Research Site:005Manchester, CT
CBCC Global Research Site:006Deerfield Beach, FL
CBCC Global Research Site:007Philadelphia, PA
CBCC Global Research Site:004Carmel, IN
More Trial Locations
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Who Is Running the Clinical Trial?
Caregen Co. Ltd.Lead Sponsor
CBCC Global ResearchCollaborator
References
Peptide redesign for inhibition of the complement system: Targeting age-related macular degeneration. [2018]To redesign a complement-inhibiting peptide with the potential to become a therapeutic for dry and wet age-related macular degeneration (AMD).
Avacincaptad pegol for geographic atrophy secondary to age-related macular degeneration: 18-month findings from the GATHER1 trial. [2023]To assess the safety and efficacy of avacincaptad pegol (ACP), a C5 inhibitor, for geographic atrophy (GA) secondary to age-related macular degeneration (AMD) over an 18-month treatment course.
The Need for Treatment of Neovascular Age-Related Macular Degeneration: A Study Based on the Polish National Registry. [2022]The Polish National AMD Therapeutic Program offered us a unique opportunity to determine the need for treatment of neovascular age-related macular degeneration (nAMD).
Changes in aqueous and vitreous inflammatory cytokine levels in neovascular age-related macular degeneration: a systematic review and meta-analysis. [2021]Inflammatory cytokines are involved in the pathogenesis of neovascular age-related macular degeneration (nAMD) and have been shown to be useful as diagnostic and predictive biomarkers. Given the heterogeneity of data within the literature, we aimed to quantitatively summarize data related to inflammatory cytokines in nAMD. A systematic search without year limitation was performed up to 13 April 2020. Studies were included if they provided data on aqueous or vitreous cytokine concentrations in patients with nAMD. Data were extracted from 95 studies that encompassed 3105 study eyes with nAMD and 1209 control eyes. Effect sizes were generated as standardized mean differences (SMDs) of cytokine concentrations between patients with nAMD and controls. Among the 4314 eyes in 95 studies, aqueous concentrations (standard mean difference, 95% confidence interval and p-value) of MCP-1 (0.43, 0.09 to 0.77 and p = 0.01), MIG (0.63, 0.31 to 0.94 and p = 0.0001), TGF-β (0.45, 0.07 to 0.82 and p = 0.02) and VEGF (0.64, 0.31 to 0.98 and p = 0.0001) were significantly higher in patients with nAMD compared to healthy controls. No differences, failed sensitivity analyses or insufficient data were found between patients with nAMD and healthy controls for the concentrations of the remaining cytokines and with all vitreous samples. Previous studies had shown conflicting associations with nAMD for all 27 cytokines assessed. Our analysis indicates multiple candidate cytokines other than VEGF that are implicated in nAMD and adds clarity to the previous literature. This will help focus translational research in nAMD investigating biomarkers and therapeutic targets.
Suppression of drusen formation by compstatin, a peptide inhibitor of complement C3 activation, on cynomolgus monkey with early-onset macular degeneration. [2022]For the past 10 years, number of evidence has shown that activation of complement cascade has been associated with age-related macular degeneration (AMD). The genome wide association study in American population with dominantly dry-type AMD has revealed strong association with single nucleotide polymorphism (SNP) of complement genes. Protein composition of drusen, a deposit observed in sub-retinal space between Bruch's membrane and retinal pigment epithelial (RPE), contains active complement molecules in human and monkey. These evidences have leaded us to consider the possibility of suppressing complement cascade in the retina to delay or reverse the onset of AMD. To test is hypothesis we used the C3 inhibitor Compstatin on primate model with early-onset macular degeneration which develop drusen in less than 2 years after birth. Our preliminary result showed drusen disappearance after 6 months of intravitreal injection.
A Novel HDL-Mimetic Peptide HM-10/10 Protects RPE and Photoreceptors in Murine Models of Retinal Degeneration. [2020]Age-related macular degeneration (AMD) is a leading cause of blindness in the developed world. The retinal pigment epithelium (RPE) is a critical site of pathology in AMD. Oxidative stress plays a key role in the development of AMD. We generated a chimeric high-density lipoprotein (HDL), mimetic peptide named HM-10/10, with anti-oxidant properties and investigated its potential for the treatment of retinal disease using cell culture and animal models of RPE and photoreceptor (PR) degeneration. Treatment with HM-10/10 peptide prevented human fetal RPE cell death caused by tert-Butyl hydroperoxide (tBH)-induced oxidative stress and sodium iodate (NaIO3), which causes RPE atrophy and is a model of geographic atrophy in mice. We also show that HM-10/10 peptide ameliorated photoreceptor cell death and significantly improved retinal function in a mouse model of N-methyl-N-nitrosourea (MNU)-induced PR degeneration. Our results demonstrate that HM-10/10 protects RPE and retina from oxidant injury and can serve as a potential therapeutic agent for the treatment of retinal degeneration.
Synthesis and structural characterization of carboxyethylpyrrole-modified proteins: mediators of age-related macular degeneration. [2021]Protein modifications in which the epsilon-amino group of lysyl residues is incorporated into a 2-(omega-carboxyethyl)pyrrole (CEP) are mediators of age-related macular degeneration (AMD). They promote both angiogenesis into the retina ('wet AMD') and geographic retinal atrophy ('dry AMD'). Blood levels of CEPs are biomarkers for clinical prognosis of the disease. To enable mechanistic studies of their role in promoting AMD, for example, through the activation of B- and T-cells, interaction with receptors, or binding with complement proteins, we developed an efficient synthesis of CEP derivatives, that is especially effective for proteins. The structures of tryptic peptides derived from CEP-modified proteins were also determined. A key finding is that 4,7-dioxoheptanoic acid 9-fluorenylmethyl ester reacts with primary amines to provide 9-fluorenylmethyl esters of CEP-modified proteins that can be deprotected in situ with 1,8-diazabicyclo[5.4.0]undec-7-ene without causing protein denaturation. The introduction of multiple CEP-modifications with a wide variety of CEP:protein ratios is readily achieved using this strategy.
Complement Factor P in choroidal neovascular membranes of patients with age-related macular degeneration. [2009]To evaluate whether complement Factor P (properdin) was present in surgically removed choroidal neovascular membranes of patients with age-related macular degeneration (AMD) and to investigate whether associated pre- and postoperative clinical characteristics can be correlated.