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About Aerie

Aerie (NASDAQ: AERI) discovers, develops, and commercializes therapies for the treatment of patients with open-angle glaucoma, ocular surface diseases, and retinal diseases. Its develops a wide variety of eye products and drops and its products include 'Rhopressa' which provides consistent intraocular pressure (IOP) reduction, 'Rocklatan' which demonstrates superiority to latanoprost in US Phase 3 trials, and 'DISCOVaerie Live' which is an interactive environment that allows sharing of information about the products. The company was founded in 2005 and is based in Durham, North Carolina. In November 2022, Aerie was acquired by Alcon.

Headquarters Location

4301 Emperor Blvd. Suite 400

Durham, North Carolina, 27703,

United States


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1,904 items

Aerie Patents

Aerie has filed 79 patents.

The 3 most popular patent topics include:

  • Amines
  • Fluoroarenes
  • Cannabinoids
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Cannabinoids, Phenols, G protein coupled receptors, Beta blockers, Clusters of differentiation


Application Date


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Related Topics

Cannabinoids, Phenols, G protein coupled receptors, Beta blockers, Clusters of differentiation



Latest Aerie News

Impact of Modifying Abicipar Manufacturing Process in Patients with Neovascular Age-Related Macular Degeneration: MAPLE Study Results

May 11, 2023

Table 5 Treatment-Related TEAEs (Safety Population) IOI in the study eye was reported in 8.9% (11/123) of the patients ( Table 6 ). The majority of patients with IOI were treatment-naïve (9 of 11); two patients (Patients 4 and 11) were previously treated. IOI was diagnosed after one injection in three study eyes, two injections in two study eyes, and four injections in six study eyes ( Table 7 ). Nine cases were reported by the investigators as mild (3, 2.4%) or moderate (6, 4.9%). Severe IOIs were reported in 1.6% (2/123) of study eyes. Ten patients with IOI were treated with topical corticosteroids upon presentation of the AE; four cases with moderate and/or severe IOI also received oral or intraocular steroids ( Table 6 ). One patient with IOI did not receive any treatment for the IOI, and the IOI fully resolved by study end. Of the two patients with severe IOI, one patient (Patient 10; Table 6 ) with iritis achieved full resolution with topical steroid treatment by study end with BCVA recovered to baseline levels. The other patient (Patient 11; Table 6 ) with panuveitis achieved full resolution with topical and oral steroids after study end with BCVA recovered to baseline levels. Of the 11 patients with reported events of IOI, the event was considered resolved for 9 patients and ongoing for 2 patients (Patients 6 and 11; Table 6 ) by study end. Both patients with ongoing IOI were treated with topical and oral steroids, were followed for safety reasons after completing the study exit visit, and achieved full resolution of IOI within 2 months post exit. One patient (Patient 1; Table 6 ) with IOI also had reported retinal hemorrhage, considered to be related to the study drug and not related to the study procedure, and vitreous hemorrhage, which was not considered to be related to the study drug or the procedure. At the week 28 exit visit, this patient’s BCVA dropped to 25 letters as a result of the hemorrhage and subsequent vitrectomy in the study eye. Visual acuity in the majority of patients with IOIs (8/11) recovered to baseline levels or better by study end. Four out of five patients with increased IOP had concurrent events of IOI. After study completion, all IOI cases completely resolved with IOP returned to the normal range, and overall vision in the majority of these patients recovered to slightly better than baseline. Table 6 Summary of Patients with IOI After Intravitreal Abicipar Injection Table 7 First IOI Relative to Abicipar Injection Cycle To evaluate the potential for abicipar to inhibit systemic VEGF action and elicit production of anti-abicipar/pegol antibodies, PK and immunogenicity testing were conducted. Serum concentrations of free abicipar were below the limit of quantification (BLQ) at baseline (day 1) in patients included in the PK analysis. Free abicipar concentrations were generally measurable in serum on day 3 following abicipar administration with mean concentrations of 0.813 ± 0.664 nM. At week 8 (predose), free abicipar concentrations were BLQ in all patients. Serum samples were analyzed for antidrug antibodies in all 123 patients. The cumulative incidence of anti-abicipar antibodies detectable in blood samples from patients receiving 2 mg abicipar was 30.1% (37/123). Titers following a single injection were low at week 4, peaked by week 12, and declined thereafter. Among patients with anti-abicipar antibodies, the median maximal titer over the duration of the study was 640 (range: 10–81,920). Following a single intravitreal injection of abicipar, the incidence of neutralizing antibodies was low (1, 0.8%). This incidence increased after 3 injections and then plateaued; the cumulative number of patients developing neutralizing antibodies at any visit was 18.7% (23/123). The incidence of anti-PEG antibodies was low and did not vary significantly throughout the course of the study. The cumulative number of patients developing anti-PEG antibodies at any visit was 2.4% (3/123). Titers were low throughout the study, and the median maximal titer over the duration of the study among patients with anti-PEG antibodies was 20 (range: 20–80). Serum samples taken from the study participants before abicipar treatment served as a negative control; no patient with an evaluable baseline serum sample tested positive for pre-existing anti-abicipar or anti-PEG antibodies. Evaluation of the impact of antidrug antibodies on AEs within this study showed no correlation between overall incidence of AEs and antidrug antibody response. The majority of patients with IOI AEs had positive anti-abicipar antibody responses postbaseline, but the majority of patients with antidrug antibodies did not develop IOI, and not all patients who developed IOI had antidrug antibodies. The relationship between immunogenicity and IOI was analyzed further. Of the patients who were positive for anti-abicipar antibodies postbaseline, 75.7% (28/37) did not have IOI. However, the majority (81.8% [9/11]) of patients with IOI AEs were positive for anti-abicipar antibodies postbaseline. In these patients, maximum titers at any visit ranged from 20 to >80,000. A higher percentage of patients (6 of 8, 75%) who had high (≥10,000) anti-abicipar titers at any visit during the study also developed IOI. However, the magnitude of the anti-abicipar response to abicipar treatment did not appear to be associated with the severity of the IOI AEs, and inflammation in patients with high titers was not necessarily deemed severe. Of the eight patients with high anti-abicipar titers (≥10,000), five patients developed IOI: one patient had severe inflammation, four patients had moderate inflammation, and three patients had no inflammation. The onset of these events and positive anti-abicipar antibody status did not appear to have a consistent temporal pattern in that an anti-abicipar response did not consistently precede, coincide with, or follow the AE. Moreover, there was no trend for a relationship between the severity of the AE and the magnitude of the anti-abicipar antibody response. Thus, a causal relationship between AEs, including IOI, and antidrug antibody response could not be established. Safety measures did not indicate any safety concerns apart from IOI. Mean changes from baseline in all laboratory test results were minimal, and a potentially clinically significant postbaseline laboratory value was reported for no more than 1 patient for each hematology and blood chemistry parameter. Similarly, there were no clinically meaningful mean changes in systolic or diastolic blood pressure or pulse rate. Findings on biomicroscopy and ophthalmoscopy generally were related to the injection procedure (eg, conjunctival hemorrhage), underlying nAMD (eg, macular edema), or IOI (eg, keratic precipitates). Vision Outcomes Stable vision was consistent and maintained for ≥95.9% (118/123) of patients at all study visits ( Figure 2 ). The proportion of patients with stable vision at week 28 (primary endpoint) was 97.6% (120/123). Vision improvement, as assessed by the proportion of patients who gained at least 10 or 15 letters from baseline, showed a similar trend of consistent results from week 4 through week 28. The proportion of patients with BCVA ≥70 letters (20/40 Snellen equivalent) also remained consistent from weeks 4 to 28. In general, mean change from baseline BCVA in number of letters demonstrated numerical improvement from weeks 4 through 28 ( Figure 3 ). The mean baseline BCVA value was 62 letters. At week 28, the mean change in BCVA from baseline was +3.6 letters (95% CI, 2.24 to 5.01). Additionally, the mean change in BCVA from baseline was numerically greater at week 28 in patients without prior anti-VEGF treatment (+4.4 letters; 95% CI, 2.67 to 6.19) compared with previously treated patients (+1.8 letters; 95% CI, −0.36 to 3.86). Figure 2 Proportion of patients with stable vision (<15-letter loss in best-corrected visual acuity from baseline) in the safety population. Missing values were imputed with the last-observation-carried-forward method. Figure 3 Mean ± standard error of the mean (SEM) change in best-corrected visual acuity (BCVA) from baseline to study end in treatment-naïve and previously treated patients who received 2 mg abicipar. Anatomic Outcomes The CRT in study eyes decreased in both previously treated and treatment-naïve eyes, and the improvement in CRT after the initial doses was maintained through week 28 ( Figure 4 ). Mean reduction in CRT was generally consistent across visits and ranged from −52.3 to −82.5 μm. Mean CRT change from baseline at week 28 was −82.5 µm (95% CI, −102.14 to −62.80). At week 28, the mean change in CRT from baseline showed greater reductions for patients without prior anti-VEGF treatment (−98.5 μm; 95% CI, −121.65 to −75.26) compared with previously treated patients (−45.5 μm; 95% CI, −81.02 to −9.98). Figure 4 Mean ± standard error of the mean (SEM) change in central retinal thickness (CRT) from baseline to study end in treatment-naïve and previously treated patients who received 2 mg abicipar. Discussion To improve the safety profile of abicipar, the drug substance manufacturing process was modified to reduce overall host-derived impurities. In vitro IIRMI assessment using PBMCs demonstrated a marked reduction in the inflammatory marker signal for the revised manufacturing process when compared with the manufacturing process employed for the investigational product used in the CEDAR and SEQUOIA studies. The MAPLE study evaluated 2 mg abicipar, produced through the modified manufacturing process, which achieved stable vision at week 28 with an improved safety profile in both treatment-naïve and previously treated patients with nAMD. IOI is a well-recognized risk of anti-VEGF injections. Optimal manufacturing, formulation, handling, and delivery of anti-VEGF biologic drug products are complex and require a commitment to continuous process improvement to ensure safety and effectiveness. Intrinsic process impurities such as E. coli host cell proteins, extrinsic impurities such as endotoxin- or syringe-associated silicone droplets, and the formulation have been implicated as causes of IOI. 25–29 In the Phase 1/2 FOCUS study, ranibizumab had an IOI rate of 38.1%. The incidence of IOIs dramatically decreased for ranibizumab following adoption of a solubilized formulation used in the ANCHOR and MARINA studies and derived from the lyophilized formulation used in FOCUS. In recent Phase 3 studies, the rate of IOI reported with ranibizumab was 8.4% (but only 0.8% reported as possibly drug-related) in the 48-week COLUMBUS-AMD study, 30 and the rate of iritis/uveitis reported with aflibercept was <1% in the 48-week HAWK and HARRIER studies. 31 In the MAPLE study, reduction in the incidence and severity of IOI was achieved consistent with removal of pro-inflammatory impurities from the drug, but the rate of IOI (8.9%) remained higher than has been reported in recent Phase 3 studies of approved anti-VEGF therapies. The modified manufacturing process used for abicipar production, enabled by high-resolution chromatography purification methodology and sophisticated analytical methodology, allowed the removal of host-derived impurities, specifically host cell proteins. The overall IOI rate in MAPLE was 8.9% (11 of 123 patients)—a reduction from the 13.1% (96 of 625 patients on Q8 regimen) IOI rate reported in the Phase 3 pivotal studies; the rate of severe IOI TEAEs in MAPLE was 1.6% (2 of 123 patients) compared with 3.4% (21 of 625 patients on Q8 dosing schedule) through 28 weeks of follow-up in the combined Phase 3 trials. The majority of IOI TEAEs reported in MAPLE were mild to moderate (9 of 11) and treated with topical and/or oral corticosteroids upon presentation of the AE. One patient did not receive any treatment and had full resolution of the IOI. All 11 IOI cases in MAPLE completely resolved, and overall vision recovered to better than baseline; 9 cases resolved by study end with the remaining 2 achieving full resolution within 2 months after study end. No cases of endophthalmitis or retinal vasculitis were reported in the MAPLE study. However, further reduction of IOI is necessary for abicipar to achieve an IOI incidence in line with other anti-VEGF biologics. The cause of IOI is likely multifactorial for any drug. The different considerations for potential causes are depicted in Figure 5 . Emerging evidence indicates that the syringe, needle, and silicone oil content can contribute to eliciting IOI and was recently reviewed by Melo et al. 32 Thus, in addition to the drug manufacturing process, the product presentation components must also be carefully considered to minimize IOI. Figure 5 Multifactorial considerations for the potential causes of intraocular inflammation. Images created with Abbreviation: CMC, Chemistry, Manufacturing and Controls. Vision and anatomic outcomes in the MAPLE study showed a clinically meaningful improvement in BCVA and CRT, in line with previous results in the CEDAR and SEQUOIA studies. In MAPLE, stable vision was maintained for ≥95.9% of patients at all study visits, the mean BCVA improved by 3.6 letters and the mean CRT decreased by 82.5 µm from baseline to week 28 with 86.2% of patients receiving 5 injections. The difference in vision and anatomic outcomes at week 28 in MAPLE and the CEDAR and SEQUOIA Phase 3 trials can be explained by differences in baseline BCVA and CRT. The mean baseline BCVA and CRT of patients in MAPLE was 62 letters and 353.1 µm compared with 56.8 letters and 382.5 µm in the CEDAR and SEQUOIA abicipar Q8 population. Patients in MAPLE may have experienced a ceiling effect, as patients with higher initial BCVA and thinner CRT typically achieve less BCVA gain and CRT reduction than individuals with more significant BCVA loss and thicker CRT (eg, patients in CEDAR/SEQUOIA). Despite having better baseline vision and anatomic characteristics, study eyes in MAPLE showed clinically relevant improvements in the mean change from baseline BCVA and CRT in both treatment-naïve and previously treated populations (3.6 letters gain in BCVA and 82.5 µm reduction in CRT). Limitations of the MAPLE study come from its open-label, single-arm design, which did not include comparator or placebo arms. Differences in the study populations between the MAPLE and CEDAR/SEQUOIA studies potentially could also have contributed to the observed reduction in the rate of IOI. Additionally, patient assessments were not confirmed by an independent reading center, but patients were examined by the same investigator at the screening visit and at every treatment and evaluation visit. MAPLE included both treatment-naïve and previously treated study eyes, making it difficult to compare results from this study to results from other clinical trials that only enrolled treatment-naïve patients. However, the patient population in MAPLE is more representative of a real clinic setting, allowing critical insights for retina specialists on the management of nAMD in patients with prior anti-VEGF treatment. Conclusions The MAPLE study evaluated abicipar, produced through a modified manufacturing process, in both treatment-naïve and previously treated patients with nAMD and demonstrated a moderate reduction in IOI rate compared with the Phase 3 CEDAR and SEQUOIA trials, with an IOI rate of 8.9% observed in MAPLE. Use of abicipar produced through a modified manufacturing process was associated with favorable functional and anatomical outcomes, while lessening the treatment burden for patients maintained on a Q8 treatment regimen or those on a treat-and-extend regimen that may require more visits than a predictable fixed dosing schedule. To fully realize the potential of abicipar as a treatment for nAMD, further reduction of IOI should be achieved. Abbreviations Abicipar, abicipar pegol; AE, adverse event; BCVA, best-corrected visual acuity; BLQ, below the limit of quantification; CI, confidence interval; CNV, choroidal neovascularization; CRT, central retinal thickness; ETDRS, Early Treatment Diabetic Retinopathy Study; IIRMI, innate immune response modulating impurity; IL-1β, interleukin-1 beta; IL-6, interleukin 6; IOI, intraocular inflammation; IOP, intraocular pressure; LOCF, last observation carried forward; LPS, lipopolysaccharide; MedDRA, Medical Dictionary for Regulatory Activities; nAMD, neovascular age-related macular degeneration; PBMC, peripheral blood mononuclear cell; PBS, phosphate-buffered saline; PEG, polyethylene glycol; Q4, monthly; Q8, every 8 weeks following three loading doses; Q12, every 12 weeks following three loading doses; RPMI, Roswell Park Memorial Institute; SD-OCT, spectral-domain optical coherence tomography; TEAE, treatment-emergent adverse event; TNF-α, tumor necrosis factor-alpha; VEGF, vascular endothelial growth factor. Data Sharing Statement AbbVie is committed to responsible data sharing regarding the clinical trials we sponsor. This includes access to anonymized, individual, and trial-level data (analysis data sets), as well as other information (eg, protocols, clinical study reports, or analysis plans), as long as the trials are not part of an ongoing or planned regulatory submission. This includes requests for clinical trial data for unlicensed products and indications. These clinical trial data can be requested by any qualified researchers who engage in rigorous, independent, scientific research, and will be provided following review and approval of a research proposal, Statistical Analysis Plan (SAP), and execution of a Data Sharing Agreement (DSA). Data requests can be submitted at any time after approval in the US and Europe and after acceptance of this manuscript for publication. The data will be accessible for 12 months, with possible extensions considered. For more information on the process or to submit a request, visit the following link: . Acknowledgments AbbVie and the authors thank the investigators and patients who participated in the MAPLE study, and Dr Swati Gupta (AbbVie) and Dr Joe Zhou (former employee of Allergan) for conducting the in vitro PBMC studies. Nayna Sanathara, PhD, of AbbVie Inc., provided medical writing assistance for the development of this publication. Editorial support was provided by Evidence Scientific Solutions, Inc. (Philadelphia, PA) and funded by AbbVie. All authors had access to relevant data and participated in the drafting, review, and approval of this publication. No honoraria or payments were made for authorship. DARPin is a registered trademark of Molecular Partners (Zurich, Switzerland). This work was presented in part at the following congresses: American Society of Retina Specialists, July 30, 2019, Chicago, Illinois; Bascom Palmer Eye Institute – Angiogenesis, February 8, 2020, Miami, Florida; Macula Society, February 21, 2020, San Diego, California; Association for Research in Vision and Ophthalmology, June 4, 2020 (virtual meeting); and American Society of Retina Specialists, July 24, 2020 (virtual meeting). Funding This study was sponsored by Allergan plc (Dublin, Ireland; prior to acquisition by AbbVie Inc). Allergan/AbbVie participated in the design of the study, data management, data analysis, interpretation of the data, and preparation, review, and approval of the manuscript. Disclosure David Callanan serves as a consultant for Allergan (an AbbVie company), Applied Genetic Technologies Corporation, EyePoint, Eyevensys, Graybug, Regenerative Patch Technologies, and Takeda; is on the Speaker’s Bureau for Allergan (an AbbVie company); has received research support from Aerie, Amgen, Diopsys, Eyevensys, Genentech/Roche, Gilead, Ionis, and Regeneron; and is an equity holder and employee of Aviceda Therapeutics. Rahul N. Khurana serves as a consultant for Apellis, Bausch + Lomb, Genentech, NGM Biopharmaceuticals, and Ophthea; and has received grant support from Apellis, Chengdu Kanghong, Clearside Biomedical, Eyepoint, Genentech, NGM Biopharmaceuticals, Ophthea, Oxurion, and RegenXBio. Raj Maturi serves as a consultant to and has received grants from Aerpio, AiViva, Allegro, Allergan (an AbbVie company), Allgenesis, Astellas, Boehringer Ingelheim, Clearside, Dutch Ophthalmic, Eli Lilly, Genentech, Gemini, GlaxoSmithKline, Graybug, Gyroscope, Jaeb Center for Health Research, Kalvista, NGM Biopharmaceuticals, Neurotech, Novartis, Ophthea, Oxurion, Ribomic, Roche, Samsung, Santen, Senju, ThromboGenics and Unity. Sunil Patel serves as a consultant for AiViva, Allergan (an AbbVie company), Allgenesis, Genentech-Roche, Kala, Kodiak Sciences; is on an advisory board for Allergan (an AbbVie company), Genentech-Roche, and Kodiak Sciences; has received research support from Aerie, Aerpio, Allergan, Allgenesis, Apellis, Boehringer Ingelheim, Chengdu Kanghong, Clearside, Eyepoint, Genentech-Roche, Ionis Pharmaceuticals, Iveric Bio, KalVista, Kodiak Sciences, Mylan, Novartis, Oculis, Opthea, Ophthotech, Ora, Oxurion, Regeneron, Samsung, SmileBiotek, Stealth Biotherapeutics, ThromboGenics, and Xbrane Biopharma; and has received personal fees from AiViva, Kala, Ocugenix, and RegenxBio, outside the submitted work; he is also the Chief Medical Officer and stock owner of Allgenesis Biotherapeutics, Inc. Charles C. Wykoff is a consultant for 4DMT, Adverum, Aerie Pharmaceuticals, AGTC, Alcon, Alimera, Allergan (an AbbVie company), Allgenesis, Alnylam, Annexon, Apellis, Arrowhead Pharmaceuticals, Bausch + Lomb, Bayer, Bionic Vision Technologies, Boehringer Ingelheim, Cholgene, Clearside, Curacle, Chengdu Kanghong Biotechnologies, Clearside Biomedical, EyePoint Pharmaceuticals, Foresite, Frontera, Genentech/Roche, Gyroscope, IACTA, Iveric Bio, Janssen, Kato Pharmaceuticals, Kiora, Kodiak Sciences, Kriya, Merck, Nanoscope, NGM Biopharmaceuticals, Notal Vision, Novartis, OccuRx, Ocular Therapeutix, Ocuterra, OliX, ONL Therapeutics, Opthea Limited, Oxurion, Palatin, PerceiveBio, Perfuse, PolyPhotonix, Ray, RecensMedical, Regeneron, Resonance, REGENXBIO, Roche, SAI MedPartners, SciNeuro, Stealth, Surrozen, Takeda, THEA, TissueGen, Valo, and Verana Health; has received research support from 4DMT, Adverum, Aerie Pharmaceuticals, Aldeyra, Aerpio, AffaMed, Alexion, Alimera Sciences, Alkahest, Allergan (an AbbVie company), Allgenesis, Amgen, Annexin, Annexon, Apellis, Arctic Vision, Asclepix, Bayer, Boehringer Ingelheim, Chengdu Kanghong Biotechnologies, Clearside Biomedical, EyePoint, Gemini Therapeutics, Genentech/Roche, GlaxoSmithKline, Graybug Vision, Gyroscope, IONIS Pharmaceuticals, iRENIX, Iveric Bio, Kodiak Sciences, LMRI, Nanoscope, Neurotech Pharmaceuticals, NGM Biopharmaceuticals, Novartis, Ocular Therapeutix, Ocuphire, OcuTerra, Ophthotech, Opthea, Outlook Therapeutics, Oxurion, Oxular, Oyster Point, PerceiveBio, RecensMedical, Regeneron, REGENXBIO, Roche, SamChunDang Pharm, Sandoz, Senju, Taiwan Liposome Company, UNITY, Verily, and Xbrane BioPharma; and has stock options for ONL Therapeutics, PolyPhotonix, RecensMedical, TissueGen, and Visgenx. David Eichenbaum is a consultant for Alimera Sciences, Allergan (an AbbVie company), Apellis, Bausch + Lomb, Coherus, Crinetics, the Dutch Ophthalmic Research Center, EyePoint, Genentech, Gyroscope Therapeutics Limited, Iveric Bio, KKR, Kodiak Sciences, Novartis, Ocular Therapeutix, Opthea, Outlook, RecensMedical, Regeneron, Regenxbio, ReVive, US Retina, and Vial; has served as an investigator for 4DMT, Alexion, Alkahest, Allegenesis, Annexon, AsclepiX, Bayer, Chengdu Kanghong Biotechnologies, EyePoint, Gemini, Genentech, Gyroscope Therapeutics Limited, Ionis, Iveric Bio, Kodiak Sciences, Mylan, NGM Biopharmaceuticals, Novartis, Ocular Therapeutics, Opthea, RecensMedical, Regeneron, Regenxbio, and Unity; has received speaker fees from Allergan (an AbbVie company), Apellis, Bausch + Lomb, Bayer, the Dutch Ophthalmic Research Center, EyePoint, Genentech, and Novartis; has received personal fees from Alimera and Samsama; has received grants from 4DMT, Alexion, Alkahest, Allegenesis, Annexon, AsclepiX, Aviceda, Chengdu, EyePoint, Gemini, Genentech, Gyroscope, Ionis, IvericBio, Kodiak, Mylan, NGM, Novartis, Ocular Therapeutix, Opthea, RecensMedical, Regeneron, RegenxBio, and Unity, outside the submitted work; holds equity and/or stocks for Boston Image Reading Center, Clearside Biomedical, Hemera Biopharmaceuticals, Network Eye, ReVive, and US Retina; and founded Network Eye. Arshad Khanani is a consultant for Adverum, Aerpio, Allergan (an AbbVie company), Chengdu Kanghong, DORC International, Genentech, Kato, Kodiak, Novartis, Gemini Therapeutics, Gyroscope, Iveric Bio, Opthea, Oxurion, RecensMedical, Regenxbio, and Roche; has received research support from Adverum, Allergan (an AbbVie company), Chengdu Kanghong, Gemini Therapeutics, Genentech, Gyroscope, Iveric Bio, Kodiak, NGM Bio, Novartis, Opthea, Oxurion, RecensMedical, Regenxbio, and Roche; and has received speaker fees from Allergan (an AbbVie company) and Novartis. Tarek Hassan is a consultant for Allergan (an AbbVie company), Aviceda, Bayer, EyePoint, Genentech, Iveric Bio, Novartis, Regeneron, and Roche. Hanh Badger, Shraddha Mehta, Grace Le, and Xiao-Yan Li were employees of Allergan plc at the time of the study. Mayssa Attar and Jennifer Seal are employees of AbbVie and may hold stock/stock options. The authors report no other conflicts of interest in this work. References 1. Ding X, Patel M, Chan -C-C. Molecular pathology of age-related macular degeneration. Prog Retin Eye Res. 2009;28(1):1–18. doi:10.1016/j.preteyeres.2008.10.001 2. Cheung LK, Eaton A. Age-related macular degeneration. Pharmacotherapy. 2013;33(8):838–855. doi:10.1002/phar.1264 3. Ciulla TA, Rosenfeld PJ. Antivascular endothelial growth factor therapy for neovascular age-related macular degeneration. Curr Opin Ophthalmol. 2009;20(3):158–165. doi:10.1097/ICU.0b013e32832d25b3 4. Grisanti S, Tatar O. The role of vascular endothelial growth factor and other endogenous interplayers in age-related macular degeneration. Prog Retin Eye Res. 2008;27(4):372–390. doi:10.1016/j.preteyeres.2008.05.002 5. Shirley M. Faricimab: first approval. Drugs. 2022;82(7):825–830. doi:10.1007/s40265-022-01713-3 6. Vabysmo prescribing information. Available from: . Accessed

Aerie Frequently Asked Questions (FAQ)

  • When was Aerie founded?

    Aerie was founded in 2005.

  • Where is Aerie's headquarters?

    Aerie's headquarters is located at 4301 Emperor Blvd., Durham.

  • What is Aerie's latest funding round?

    Aerie's latest funding round is Acq - P2P.

  • How much did Aerie raise?

    Aerie raised a total of $71M.

  • Who are the investors of Aerie?

    Investors of Aerie include Alcon, Novo Ventures, Alta Partners, TPG Biotech, Sofinnova Ventures and 5 more.

  • Who are Aerie's competitors?

    Competitors of Aerie include Longevica, Ripple Therapeutics, Noveome Biotherapeutics, Hawaii Biotech, PhaseBio Pharmaceuticals, Hemarina, BioMarck Pharmaceuticals, Aduro BioTech, Potentia Pharmaceuticals, ViroPharma and 18 more.

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