Publications

@article{Panos2023-mp,

title = {Faricimab: Transforming the future of macular diseases treatment 

 - A comprehensive review of clinical studies},

author = {Georgios D Panos and Arun Lakshmanan and Panagiotis Dadoukis and Matteo Ripa and Lorenzo Motta and Winfried M Amoaku},

year  = {2023},

date = {2023-09-01},

journal = {Drug Des. Devel. Ther.},

volume = {17},

pages = {2861\textendash2873},

publisher = {Informa UK Limited},

abstract = {Degenerative eye conditions such as age-related macular 

 degeneration (AMD), diabetic retinopathy, and retinal vein 

 occlusion are major contributors to significant vision loss in 

 developed nations. The primary therapeutic approach for managing 

 complications linked to these diseases involves the intravitreal 

 delivery of anti-vascular endothelial growth factor (VEGF) 

 treatments. Faricimab is a novel, humanised, bispecific antibody 

 that simultaneously binds all VEGF-A isoforms and 

 Angiopoietin-2, which has been approved by regulatory agencies, 

 such as the US Food and Drug Administration (FDA), the UK 

 Medicines and Healthcare products Regulatory Agency (MHRA) and 

 the European Medicines Agency (EMA), for the treatment of 

 neovascular AMD and diabetic macular oedema (DMO). Intravitreal 

 faricimab holds the promise of reducing the treatment burden for 

 patients with these conditions by achieving comparable or 

 superior therapeutic outcomes with fewer clinic visits. The 

 scope of faricimab's application includes addressing complex 

 macular conditions such as DMO. This review intends to elucidate 

 the distinctive pharmacological characteristics of faricimab and 

 provide an overview of the key clinical trials and real-world 

 studies that assess its effectiveness and safety in treating 

 degenerative macular diseases.},

keywords = {age-related macular degeneration, anti-VEGF, degenerative   macular disorders, diabetic   retinopathy, diabetic macular oedema, efficacy, faricimab, intravitreal treatment, retinal vein occlusion, safety},

pubstate = {published},

tppubtype = {article}

}

@article{Titi-Lartey2022-jg,

title = {Toll-like receptor signalling pathways and the pathogenesis of 

 retinal diseases},

author = {Owuraku Titi-Lartey and Imran Mohammed and Winfried M Amoaku},

year  = {2022},

date = {2022-03-01},

journal = {Front. Ophthalmol. (Lausanne)},

volume = {2},

pages = {850394},

publisher = {Frontiers Media SA},

abstract = {There is growing evidence that the pathogenesis of retinal 

 diseases such as diabetic retinopathy (DR) and age-related 

 macular degeneration (AMD) have a significant chronic 

 inflammatory component. A vital part of the inflammatory cascade 

 is through the activation of pattern recognition receptors (PRR) 

 such as toll-like receptors (TLR). Here, we reviewed the past 

 and current literature to ascertain the cumulative knowledge 

 regarding the effect of TLRs on the development and progression 

 of retinal diseases. There is burgeoning research demonstrating 

 the relationship between TLRs and risk of developing retinal 

 diseases, utilising a range of relevant disease models and a few 

 large clinical investigations. The literature confirms that TLRs 

 are involved in the development and progression of retinal 

 diseases such as DR, AMD, and ischaemic retinopathy. Genetic 

 polymorphisms in TLRs appear to contribute to the risk of 

 developing AMD and DR. However, there are some inconsistencies 

 in the published reports which require further elucidation. The 

 evidence regarding TLR associations in retinal dystrophies 

 including retinitis pigmentosa is limited. Based on the current 

 evidence relating to the role of TLRs, combining anti-VEGF 

 therapies with TLR inhibition may provide a longer-lasting 

 treatment in some retinal vascular diseases.},

keywords = {age-related macular degeneration, diabetic retinopathy, genetic   polymorphisms, inflammation, ischaemic retinopathy, retinal   diseases, retinal dystrophies, toll-like receptors},

pubstate = {published},

tppubtype = {article}

}