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VykaT XR (Diazoxide Choline) Gets FDA Approval for Prader-Willi Syndrome-Related Hyperphagia

by with No Comment Disease & Drugs

Written by Pavan Reddy (Biomedical Engineer) and Pragati Ekamalli (B.Pharm)

Reviewed and Fact Checked by Vikas Londhe M.Pharm (Pharmacology)

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Introduction
The U.S. Food and Drug Administration (FDA) have recently approved VykaT XR (diazoxide choline extended-release) for the treatment of hyperphagia an insatiable hunger and food-seeking behaviour—in patients with Prader-Willi Syndrome (PWS). This marks a significant milestone in addressing one of the most challenging and life-threatening aspects of PWS.

Understanding Prader-Willi Syndrome and Hyperphagia

Prader-Willi Syndrome is a rare genetic disorder characterized by hypotonia, developmental delays, behavioural challenges, and endocrine abnormalities. One of the most debilitating symptoms is hyperphagia, an extreme and unrelenting hunger that can lead to severe obesity, diabetes, and life-threatening complications if not carefully managed.

Hyperphagia in Prader-Willi Syndrome (PWS) is a hallmark symptom and one of the most challenging aspects of the condition to manage.

Hyperphagia refers to an abnormally increased appetite for and consumption of food. In PWS, this goes beyond typical overeating — it’s a compulsive drive to eat that often leads to life-threatening obesity if not carefully managed.

Prader-Willi Syndrome is a complex genetic disorder caused by the loss of function of specific genes on chromosome 15 (most often from the paternal side). One of the primary areas affected is the hypothalamus, the brain region responsible for regulating hunger and satiety.

Because of this hypothalamic dysfunction:

Individuals with PWS don’t receive normal signals of fullness.

Ghrelin, the “hunger hormone,” is often found at abnormally high levels.

This creates a constant feeling of hunger, regardless of how much food is consumed.

PWS-related eating behaviour typically progresses in stages:

Infancy – Poor muscle tone (hypotonia) and feeding difficulties, often requiring tube feeding.

Early Childhood (2–4 years) – Weight gain begins without an apparent increase in food intake.

Later Childhood – An insatiable appetite emerges; the drive to eat intensifies, often leading to food-seeking behaviors, hoarding, and even food theft.

Until now, treatment options for hyperphagia have been limited tostrict dietary supervision, behavioural therapy, and growth hormone therapy (which help with some symptoms but do not directly address hyperphagia).

VykaT XR offers the first FDA-approved pharmacological treatment specifically targeting this symptom.

What is VykaT XR (Diazoxide Choline)?

Diazoxide choline is a salt form of diazoxide, a medication that has been around for decades, primarily used to treat conditions like hypoglycemia (low blood sugar) due to its ability to inhibit insulin secretion and hypertension (high blood pressure). The choline salt form is designed to potentially improve the bioavailability and tolerability of diazoxide, especially in oral formulations.

VykaT XR is an extended-release formulation of diazoxide choline, a modified version of diazoxide.

Key Benefits of VykaT XR

Reduces excessive hunger by acting on brain pathways involved in appetite regulation.

Extended-release formulation allows for once-daily dosing, improving compliance.

Potential to improve quality of life by reducing food-related anxiety and obsessive behaviors.

Clinical Trials and Efficacy

The approval of VykaT XR was based on data from Phase 3 clinical trials demonstrating its effectiveness in reducing hyperphagia symptoms. Key findings included

The C602-RWP (Randomized Withdrawal Period) was a phase of the C602 clinical study evaluating the efficacy and safety of Diazoxide Choline Extended-Release (DCCR) tablets for treating Prader-Willi Syndrome (PWS). This phase was specifically assessed the impact of discontinuing DCCR on hyperphagia-related behaviors in individuals with PWS.

Study design includes 77 individual participants with PWS who had previously been enrolled in the C602 open-label extension study and had received DCCR treatment for two to four years. Participants were randomized in a 1:1 ratio to either continue DCCR treatment or switch to a placebo for duration of 16 weeks. Primary Endpoint include Change from baseline in hyperphagia-related behaviors, measured using the Hyperphagia Questionnaire for Clinical Trials (HQ-CT).

Key Findings of the trial in hyperphagia Assessment at week 16, participants who switched to placebo showed a significant worsening in hyperphagia-related behaviors, with an increase of 5.0 points in the HQ-CT total score compared to those who continued DCCR treatment

Secondary endpoints, including the Clinical Global Impression of Severity (CGI-S) and Clinical Global Impression of Improvement (CGI-I), indicated trends toward worsening conditions in the placebo group compared to the DCCR group.

DCCR was generally well-tolerated, with no new or unexpected safety signals reported during the randomized withdrawal period.​

These results suggest that continuous treatment with DCCR may be beneficial in managing hyperphagia in individuals with PWS, and discontinuation could lead to a significant worsening of symptoms. Based on these findings, Soleno Therapeutics planned to submit a New Drug Application (NDA) to the U.S. Food and Drug Administration (FDA).

Implications for Patients and Families

For individuals with PWS and their caregivers, VykaT XR offers new hope in managing a symptom that has long been a major source of distress. Many caregivers view VykaT XR as a long-awaited option that addresses one of the most difficult aspects of PWS.

Patient advocacy groups Prader-Willi Syndrome Association USA have shared cautiously optimistic statements, emphasizing the potential impact on family dynamics, independence, and safety. However Community discussions indicate concerns about insurance coverage, cost, and provider awareness.

Conclusion

The FDA’s approval of VykaT XR represents a groundbreaking advancement in the treatment of Prader-Willi Syndrome. While ongoing research will further define its long-term benefits and safety profile, this therapy provides a much-needed tool in managing hyperphagia a symptom that profoundly impacts the lives of those with PWS.

Patients and healthcare providers are encouraged to discuss VykaT XR as part of a comprehensive PWS management plan, which should continue to include nutritional support, behavioural interventions, and endocrine care.

For now, VykaT XR stands as a landmark therapy, offering new possibilities for individuals and families affected by Prader-Willi Syndrome.

References

  1. US FDA approval of VykaT XR, Soleno Therapeutics, 26 March 2025, available from https://investors.soleno.life/static-files/9e8f0f73-ea3b-47fe-8c8e-fbd276a31333
  2. Soleno therapeutics announces U.S. FDA approval of VykaT XR to treat hyperphagia in Prader-Willi Syndrome, Soleno Therapeutics, 26 March 2025, available from https://investors.soleno.life/news-releases/news-release-details/soleno-therapeutics-announces-us-fda-approval-vykattm-xr-treat
  3. Driscoll DJ, Miller JL, Cassidy SB. Prader-Willi Syndrome. 1998 Oct 6 [Updated 2024 Dec 5]. In: Adam MP, Feldman J, Mirzaa GM, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2025. Available from: https://www.ncbi.nlm.nih.gov/books/NBK1330/

4. Prader-Willi Syndrome, Foundation for Prader Willi Research, available from https://www.fpwr.org/what-is-prader-willi-syndrome#definition

  1. Rahman QFA, Jufri NF, Hamid A. Hyperphagia in Prader-Willi syndrome with obesity: From development to pharmacological treatment. Intractable Rare Dis Res. 2023 Feb; 12(1):5-12. Doi: 10.5582/irdr.2022.01127. PMID: 36873672; PMCID: PMC9976092.
  2. S.A. Bellis, I. Kuhn, S. Adams, L. Mullarkey, A. Holland, The consequences of hyperphagia in people with Prader-Willi Syndrome: A systematic review of studies of morbidity and mortality, European Journal of Medical Genetics, Volume 65, Issue 1, 2022,104379, https://doi.org/10.1016/j.ejmg.2021.104379
  3. Holsen LM, Zarcone JR, Brooks WM, Butler MG, Thompson TI, Ahluwalia JS, Nollen NL, Savage CR. Neural mechanisms underlying hyperphagia in Prader-Willi syndrome. Obesity (Silver Spring). 2006 Jun;14(6):1028-37. Doi: 10.1038/oby.2006.118. PMID: 16861608; PMCID: PMC1535344
  4. Miller JL, Gevers E, Bridges N, et al, Diazoxide Choline Extended-Release Tablet in People With Prader-Willi Syndrome: A Double-Blind, Placebo-Controlled Trial. J Clin Endocrinol Metab. 2023 Jun 16;108(7):1676-1685. Doi: 10.1210/clinem/dgad014. PMID: 36639249; PMCID: PMC10271219.

9. Vykat XR FDA Approval History, Drugs.com, available from https://www.drugs.com/history/vykat-xr.html

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No More Implants? Lab-Grown Teeth Might Be the Future of Dentistry

by with No Comment Disease & Drugs

Written By Yogita Bhadane B.Pharm

Reviewed and Fact Checked By Vikas Londhe M.Pharm (Pharmacology)

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Lost tooth has been a challenge in oral healthcare since log time; it has been often treated with artificial replacements like implants or dentures. But what if an idea of re-growing tooth outside body became real? A recent study published in ACS Macro Letters brings this idea closer to reality by using advanced hydrogel-based matrix to grow tooth organoids miniature, a lab-grown versions of developing teeth.

Introduction: Why We Need Biological Tooth Replacement

Tooth loss can happen for many reasons, like decay, gum disease, injury, or illness. Missing teeth can hurt a person’s confidence, speech, and health. Current solutions like dental implants and dentures can replace teeth, but they cannot create real tooth tissue or fully restore how a natural tooth works.

Regenerative dentistry, a field focused on regenerating and repairing an oral tissue in event of damage by stimulating a body’s natural processes instead of merely replace it, is aims to fill this gap by creating bioengineered teeth using living cells and materials that mimic how natural teeth develop. A key step in this work is making tooth organoids, which are 3D models that copy how teeth grow.

Conventional Methods for Tooth Repair and Their Limitations

Traditionally, broken or missing teeth are fixed with; fillings and crowns to rebuild structure, bridges or removable dentures to replace teeth and dental implants that attach to the jawbone.

Although implants are widely used, they are not biological. They do not grow or heal and can fail due to infection or other issues. Also, implants do not interact with surrounding tissues like real teeth.

Attempts to engineer teeth in the lab

Researchers have tried to create teeth in the lab using materials like collagen matrix, decellularized tooth buds and synthetic polymers like PLGA, PGA, PLLA and Matrigel. However, these materials provide structure but lack tunable physical properties. Also they don’t provide enough information on how physical factors like stiffness affect tooth growth.

The New Approach: Engineering a Better Matrix for Tooth Growth

In this revolutionizing study, scientists created a tunable hydrogel system to help as a matrix to teeth grow. They modified gelatine and cross linked using the inverse-electron demand Diels−Alder reaction with specific chemical group’s in between Tetrazine (Tz) and Norbornene (Nb). By modifying the gelatine concentration (8% or 12%) and Tz: Nb ratio (1:1 or 0.5:1), they created hydrogels with different properties. These hydrogels were soft, able to swell, and stable for growing cells.

Tooth Organoid generation

To make tooth organoids, researchers took dental epithelial and mesenchymal cells from embryonic mouse tooth germs and mixed them into the hydrogel matrix to form cell pellets. They then cultured these cells in vitro for 8 days to form tooth organoids.

 How Teeth were Regrown in the Lab

Three different hydrogel types were tested:

  1. GEL_8%_R05: 8% Tz: Nb ratio 0.5:1
  2. GEL_8%_R1: 8% Tz: Nb ratio 1:1
  3. GEL_12%_R05: 12% gelatin, Tz: Nb ratio 0.5:1

Only the GEL_8%_R05 group consistently produced well-structured tooth organoids that looked like natural teeth. The study showed that the softness of the hydrogel was important for the cells to self-organize into tooth-like structures.

Implications and Future Steps

This research is a big step for regenerative dentistry. It helps us understand how teeth develop and allows for customized hydrogels that can be used to study tooth formation.

Improved understanding of dental embryogenesis, by replicating the process in controllable lab conditions

Personalized dental therapies: In the future, patient-specific cells could be used to regrow teeth in customized hydrogels.

However Xuechen Zhang one of the researchers says that “We have different ideas to put the teeth inside the mouth. We could transplant the young tooth cells at the location of the missing tooth and let them grow inside mouth. Alternatively, we could create the whole tooth in the lab before placing it in the patient’s mouth. For both options, we need to start the very early tooth development process in the lab.”

Dr Ana Angelova Volponi, King’s College London, added that “as the field progresses, the integration of such innovative techniques hold the potential to revolutionise dental care, offering sustainable and effective solutions for tooth repair and regeneration.

Next steps of the research includes use of human cells to move towards clinical translation, testing how well these organoids grow over time, adding growth factors to guide development, and exploring the possibility of transplanting mature organoids into living models.

Conclusion

In conclusion, this study shows that the mechanical properties of hydrogels are important for developing tooth organoids in the lab. By adjusting the stiffness and make-up of the matrix, researchers were able to help cells communicate and organize themselves, closely resembling natural tooth development.

References:

1. Lab-grown teeth might become an alternative to fillings following research breakthrough, Kings College London, 14 April 2025, available from https://www.kcl.ac.uk/news/lab-grown-teeth-might-become-an-alternative-to-fillings-following-research-breakthrough

2. Zhang X, Contessi Negrini N, Correia R, Sharpe PT, Celiz AD, Angelova Volponi A. Generating Tooth Organoids Using Defined Bioorthogonally Cross-Linked Hydrogels. ACS Macro Lett. 2024 Dec 17;13(12):1620-1626. Doi: 10.1021/acsmacrolett.4c00520. Epub 2024 Nov 12. PMID: 39532305; PMCID: PMC11656705

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“Age-Related Macular Degeneration: What’s New in Treatment and Research?”

by with No Comment Disease & Drugs

Medically Reviewed by Dr. Mayur Jawale (MBBS, MS- Ophthalmology, Fellowship in Phacoemulsification)

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Introduction 

Age-related macular degeneration (AMD) creates haziness on central vision and is a leading cause of irreversible vision loss in individuals over 50. It affects the macula, the central part of the retina responsible for sharp, detailed vision. AMD is affecting central vision without causing complete blindness. This can make everyday activities such as reading, driving, recognizing faces, and detailed tasks much more challenging. While there is no cure for AMD, recent advancements in medical research have led to groundbreaking treatments that slow disease progression and, in some cases, restore vision. This article explores the latest innovations in AMD therapy, including gene therapy; stem cell treatments, and novel drug delivery systems.

Types of AMD

Age-related macular degeneration (AMD) is classified into two main forms: dry (atrophic) AMD and wet (neovascular) AMD. They differ in progression, symptoms, and treatment approaches.

Dry AMD (Non-Exudative or Atrophic AMD)

Most common type (about 80-90% of AMD cases)

Slow progression over years, leading to gradual central vision loss.

Caused by thinning of the macula and accumulation of drusen (yellow protein deposits) under the retina

Advanced stage: Geographic atrophy (GA), where retinal cells degenerate, causing permanent blind spots

Current treatments: No cure, but AREDS2 supplements may slow progression

Wet AMD (Exudative or Neovascular AMD)

Less common but more severe (10-15% of AMD cases)

Rapid progression, often leading to sudden vision loss

Caused by abnormal blood vessel growth (choroidal neovascularisation) that leak fluid/blood, damaging the macula

Symptoms: Distorted vision (metamorphopsia), dark spots, rapid central vision decline

Treatments: Anti-VEGF injections (e.g., Lucentis, Eylea), laser therapy, and photodynamic therapy

Current Standard Treatments 

Before delving into new advancements, it’s essential to understand the existing treatments: 

Anti-VEGF Injections – The gold standard for wet AMD, these drugs (e.g., ranibizumab, aflibercept, bevacizumab) block vascular endothelial growth factor (VEGF), preventing abnormal blood vessel growth. No clinically major variation in the effectiveness and safety of different anti-VEGF treatments.

Laser Therapy – Laser photocoagulation is a type of laser therapy Used in certain cases of wet AMD to destroy abnormal blood vessels.

Laser photocoagulation is only used in wet AMD, where irregular blood vessels develop, but it’s not suitable for all patients.”

Vitamin Supplements (AREDS2 Formula): According to the NIH-funded AREDS2 research, taking certain vitamin and mineral supplements reduces the risk of dry AMD progressing to sight-threatening stages by 25 percent.

This formula involve Vitamin C: 500 mg, Vitamin E: 400 IU, Zinc: 80 mg (as zinc oxide), Copper: 2 mg (as cupric oxide), Lutein: 10 mg, Zeaxanthin: 2 mg

While effective, these treatments have limitations, such as frequent injections and incomplete efficacy in dry AMD. Researchers are now developing next-generation therapies to overcome these challenges. 

Cutting-Edge Advancements in AMD Treatment 

Gene Therapy for AMD 

Gene therapy is emerging as a promising approach for treating age-related macular degeneration (AMD), particularly its neovascular (wet) form. Traditional treatments for wet AMD often require frequent intravitreal injections of anti-vascular endothelial growth factor (VEGF) agents to control abnormal blood vessel growth in the retina. Gene therapy aims to provide a more sustainable solution by enabling the eye to produce therapeutic proteins internally, potentially reducing or eliminating the need for repeated injections.​

Advancements in Gene Therapy for Wet AMD

RGX-314 (REGENXBIO): This therapy utilizes an adeno-associated virus (AAV) vector to deliver a gene encoding a monoclonal antibody fragment that inhibits VEGF. It is designed for subretinal or suprachoroidal delivery, with the goal of providing long-term suppression of VEGF activity. Clinical trials are ongoing to evaluate its safety and efficacy

Ixo-vec, formerly ADVM-022 (Adverum Biotechnologies): Ixo-vec employs an AAV vector to deliver a gene encoding an anti-VEGF protein. Following favourable results from Phase 1 and Phase 2 trials, Adverum is preparing to initiate Phase 3 clinical trials in the first half of 2025.

Gene Therapy for Dry AMD (Geographic Atrophy)

While much focus has been on wet AMD, gene therapy is also being explored for geographic atrophy (GA), the advanced form of dry AMD.

GT005 (Gyroscope Therapeutics): This investigational gene therapy aims to increase the production of complement factor I, a protein that regulates the complement system implicated in GA. Clinical trials are underway to assess its safety and efficacy. ​

OCU410 (Ocugen): A Phase 1/2 study is evaluating the safety and efficacy of OCU410 for GA secondary to dry AMD. The study involves randomized, sequential assignment with single masking and aims to enroll 63 patients.

Stem Cell Therapy 

Stem cell therapy is emerging as a promising avenue for treating age-related macular degeneration (AMD), particularly its dry form, known as geographic atrophy (GA). Recent advancements have led to several clinical trials aimed at evaluating the safety and efficacy of stem cell-based treatments for AMD. Scientists are focusing on replacing damaged retinal pigment epithelium (RPE) cells, which are crucial for supporting photoreceptors, the cells responsible for detecting light.

Embryonic and Induced Pluripotent Stem Cells (iPSCs) – Researchers are implanting retinal pigment epithelium (RPE) cells derived from stem cells to replace damaged tissue. 

Phase I/II Clinical Trials – One notable initiative is a Phase I/IIa clinical trial conducted by the National Eye Institute (NEI), focusing on the transplantation of autologous induced pluripotent stem cell-derived retinal pigment epithelium (iRPE) cells. This trial aims to assess the safety of implanting iRPE patches into areas adjacent to GA in patients with advanced dry AMD.

Complement Inhibitors (For Dry AMD)

Significant advancements have been made in the development of complement inhibitors for the treatment of dry age-related macular degeneration (AMD), particularly in addressing geographic atrophy (GA), an advanced form of dry AMD.​

Approved Treatments

Pegcetacoplan (Syfovre): This C3 inhibitor received approval from the U.S. Food and Drug Administration (FDA) in February 2023 for the treatment of GA. Administered via intravitreal injection every 25 to 60 days, pegcetacoplan has demonstrated a reduction in the progression of GA lesions over time. ​

Avacincaptad Pegol (Izervay): Approved by the FDA in August 2023, this C5 inhibitor is administered through monthly intravitreal injections. Clinical trials have shown that avacincaptad pegol can slow the growth of GA lesions, with its protective effect increasing over

There are multiple clinical trial are going on to investigate new complement inhibitors like NGM621, ANX007, IONIS-FB-LRx (ASO Factor B).

Sustained Drug Delivery Systems 

Reducing injection frequency is a major focus. 

 Port Delivery System (Susvimo, Roche) – A refillable implant that continuously releases ranibizumab, requiring only biannual refills. 

Extended-Release Anti-VEGF Formulations – Drugs like KSI-301 (Kodiak Sciences) use antibody biopolymers to prolong therapeutic effects. 

Artificial Intelligence (AI) in AMD Diagnosis & Monitoring 

AI is revolutionizing early detection and personalized treatment. 

Retinal Imaging Analysis – AI algorithms (e.g., IDx-DR, Optos) detect AMD progression earlier than traditional methods. 

Predictive Modelling – AI helps predict which patients will progress to advanced AMD, enabling timely intervention

Future Directions 

CRISPR Gene Editing – Potential to correct genetic mutations causing AMD. 

Bionic Retina Implants – Devices like the PRIMA implant restore partial vision in late-stage AMD. 

Conclusion 

The landscape of AMD treatment is rapidly evolving, with gene therapy, stem cells, and sustained drug delivery systems offering hope for long-term solutions. While challenges remain, these innovations promise to transform AMD management, reducing treatment burden and improving quality of life for millions. Continued research and clinical trials will be crucial in bringing these therapies to mainstream ophthalmology. 

References

Age-Related Macular Degeneration (AMD), National Eye Institute, 22 June 2021 available from https://www.nei.nih.gov/learn-about-eye-health/eye-conditions-and-diseases/age-related-macular-degeneration

Understanding Macular Degeneration, American Academy of Ophthalmology, 01 Oct 2024 available from https://www.aao.org/eye-health/diseases/amd-macular-degeneration

New Treatments for Age-Related Macular Degeneration, American Academy of Ophthalmology, 23 May 2024 available from https://www.aao.org/eye-health/tips-prevention/promising-new-treatments-amd

Hao Q, Bailey S, Anti–Vascular Endothelial Growth Factor Drugs for Age-Related Macular Degeneration: CADTH Health Technology Review [Internet]. Ottawa (ON): Canadian Agency for Drugs and Technologies in Health; 2023 Oct. Available from: https://www.ncbi.nlm.nih.gov/books/NBK598219/

Laser Photocoagulation for Age-Related Macular Degeneration, Health, Johns Hopkins Medicine, available from https://www.hopkinsmedicine.org/health/treatment-tests-and-therapies/laser-photocoagulation-for-agerelated-macular-degeneration

Joshua Dunaief, MD, PhD,  Vitamins for Age-Related Macular Degeneration: Do You Have the Correct Formula? Macular Degeneration Research, available from https://www.brightfocus.org/resource/vitamins-for-age-related-macular-degeneration-do-you-have-the-correct-formula/

Blasiak J, Pawlowska E, Ciupińska J, New Generation of Gene Therapies as the Future of Wet AMD Treatment. Int J Mol Sci. 2024 Feb 17;25(4):2386. doi: 10.3390/ijms25042386. PMID: 38397064; PMCID: PMC10888617

Khanani AM, Thomas MJ, Aziz AA, Weng CY, Danzig CJ, Yiu G, Kiss S, Waheed NK, Kaiser PK. Review of gene therapies for age-related macular degeneration. Eye (Lond). 2022 Feb;36(2):303-311. doi: 10.1038/s41433-021-01842-1. Epub 2022 Jan 11. PMID: 35017696; PMCID: PMC8807824

Gene Therapy for Age-Related Macular Degeneration, Nuffield Department of Clinical Neurosciences, available from https://www.ndcn.ox.ac.uk/research/clinical-ophthalmology-research-group/trials/amd-gene-therapy

Qin S, Dong N, Yang M, Wang J, Feng X, Wang Y. Complement Inhibitors in Age-Related Macular Degeneration: A Potential Therapeutic Option. J Immunol Res. 2021 Jul 29;2021:9945725. Doi: 10.1155/2021/9945725. PMID: 34368372; PMCID: PMC8346298

Cruz-Pimentel M, Wu L. Complement Inhibitors for Advanced Dry Age-Related Macular Degeneration (Geographic Atrophy): Some Light at the End of the Tunnel? J Clin Med. 2023 Aug 4; 12(15):5131. Doi: 10.3390/jcm12155131. PMID: 37568533; PMCID: PMC10420150

Sarkar I, Sodha SJ, Junnuthula V, Novel and investigational therapies for wet and dry age-related macular degeneration, Drug Discovery Today, Volume 27, Issue 8, 2022, Pages 2322-2332 https://doi.org/10.1016/j.drudis.2022.04.013

Tzoumas N, Riding G, Williams MA, Steel DH. Complement inhibitors for age-related macular degeneration. Cochrane Database Syst Rev. 2023 Jun 14;6(6):CD009300. Doi: 10.1002/14651858.CD009300.pub3. PMID: 37314061; PMCID: PMC10266126

Port Delivery System for AMD, American Academy of Ophthalmology, 01 Nov 2021 available from https://www.aao.org/eyenet/article/port-delivery-system-for-amd

Stewart, M. W. (2016). Extended release anti-VEGF systems: a strategy whose time has come? Or already gone? Expert Review of Ophthalmology, 11(3), 167–169 https://doi.org/10.1080/17469899.2016.1186546

Crincoli E, Sacconi R, Querques L, Querques G. Artificial intelligence in age-related macular degeneration: state of the art and recent updates. BMC Ophthalmol. 2024 Mar 15;24(1):121. Doi: 10.1186/s12886-024-03381-1. PMID: 38491380; PMCID: PMC10943791.

Gao Y, Xiong F, Xiong J, Recent advances in the application of artificial intelligence in age-related macular degeneration. BMJ Open Ophthalmol. 2024 Nov 13;9(1):e001903. Doi: 10.1136/bmjophth-2024-001903. PMID: 39537399; PMCID: PMC11580293.

Dongchun Xie, Yuxi Chen, Sihui Hu, CRISPR-based gene therapy for wet age-related macular degeneration in mouse model, Clin. Transl. Disc 2024;4:e278,Doi: 10.1002/ctd2.278