The Germany-based company, called Complement Therapeutics GmbH (), specialises in disorders that affect the part of the body's immune system called the Complement cascade.

The complement cascade is a part of the immune system that enhances the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism.

Complement cascade disorders cause various health problems, including Geographic atrophy (GA) - or late-stage dry age-related macular degeneration - a chronic eye condition that causes blindness in millions of people globally and for which there is currently no available treatment in the UK.

The Company has subsidiaries in the UK (Complement Therapeutics Ltd) and in the USA (Complement Therapeutics Inc) as well as research laboratories in Stevenage, UK. 

The financing will allow CTx to continue the development and complete a Phase Ib clinical proof of concept of its lead treatment, called CTx001, for GA.

Proceeds from the financing will also be deployed to grow its laboratory-based activities in Stevenage (UK), evaluate CTx’s additional new medicines for non-ocular indications as well as further develop the novel Complement Precision Medicine (CPM) platform.

As scientists’ understanding of the complement cascade improves, we now know that complement plays a pivotal role in disease, with new insights creating the opportunities for identifying and developing new therapeutic strategies.

Based on pioneering research of the company’s founders, Prof Simon Clark, Prof Paul Bishop and Dr Richard Unwin from 51¸£ÀûÉç, Complement Therapeutics aims to develop innovative and effective therapeutics to address unmet needs in complement mediated diseases.

Through an extensive programme of translational research the scientists have gained powerful new insights into the ways the Complement cascade works and how it is dysregulated in age-related macular degeneration.

CTx was spun out of the University of 51¸£ÀûÉç Innovation Factory with initial funding from BGV in 2021 and subsequently received €5 million seed funding in February 2022 from Forbion and BGV.

With that funding, CTx has advanced CTx001 through preclinical proof-of-concept, secured an Innovation Passport by the Medicines and Healthcare products Regulatory Agency (MHRA) and initiated a non-interventional natural history study in the UK (i-GAIN). The i-GAIN study results will help support the clinical development planning for CTx001. 

Dr Rafiq Hasan, CEO and Managing Director at Complement Therapeutics GmbH said: “With a potentially highly differentiated lead asset combined with a precision medicine approach, we are excited by the opportunity to further develop CTx001 for the treatment of GA through to the clinic. The support of this broad syndicate enables us to generate additional data demonstrating CTx001’s unique and differentiated mechanism of action, with the potential to transform the treatment landscape in geographic atrophy.�

Dr Richard Unwin, Senior Lecturer at 51¸£ÀûÉç and one of the co-founders of the company said : “This is a hugely exciting step forward which will allow us to take observations we have made in the lab here in 51¸£ÀûÉç and move them towards developing new treatments for a range of common and serious complement-mediated diseases. By combing new therapies with our bespoke precision medicine platform we have the potential to make a real difference to the lives of patients with these debilitating disorders.â€�

Publishing in the top journal and funded by the Macular Society, the researchers were able to identify early signs of the disease which could be targeted by new treatments before symptoms develop.

Scientists have long known that people with certain genes on chromosomes 1 and 10 have a 2-3-fold higher risk of developing AMD, although lifestyle factors also play a role.

The 51¸£ÀûÉç team identified higher numbers of ‘mast cells’ in the eyes of people when either of the risk genes were present, even when there were symptoms, suggesting an early mechanism in common.

They also showed the mast cells release enzymes in the back of the eye which then damage  structures underneath the retina that in time is likely to damage the retina itself.

Mast cells exist in most tissues and are one of the immune system’s  first defences against infection, especially parasitic disease and damage.

Scientists already know there are more mast cells in the choroid in people with established AMD. The current study, however, identified higher levels in people before the disease develops.

The genes on chromosome 1 are linked to a part of the immune system called the complement cascade, which is associated with a risk of  AMD.

Though the functional role of genes expressed by chromosome 10 are not known, but increased risk of AMD is.

The work was led by Prof Paul Bishop, Professor of Ophthalmology at 51¸£ÀûÉç, in collaboration with Dr Richard Unwin in 51¸£ÀûÉç and Prof Simon Clark formerly of 51¸£ÀûÉç but now based at the University of Tübingen.

Dr Unwin said: “What is really exciting about this work is that we are studying tissue from people before they have signs of the disease.

“This gives us a look into the very earliest stages, and gives us hope that we can intervene to stop the disease developing and ultimately prevent loss of vision�

The scientists used health human eye tissue donated post mortem to the 51¸£ÀûÉç Eye Tissue Repository.

They identified those who are risk of developing age-related macular degeneration based on their risk genes, and discovered underlying changes in the tissue of the otherwise healthy at-risk individuals.

They collected retinal tissue from the back of donor eyes post mortem, following removal of the cornea for transplantation.

Then they took a small sample from the macula – the part of the retina responsible for central vision - and removed the cells to leave a thin layer of membrane which supports the photoreceptors called rod and cone cells and is where disease begins.

They analysed the proteins present in the membrane from 30 people using mass spectrometry, which identifies protein components based on their mass, to find differences in the tissue make-up between those with and without genetic risk of AMD.

The mass spectrometry, identified a series of enzymes which are made almost exclusively by mast cells, a type of immune cell.

Examining tissue from a further 53 people, they observed higher levels of mast cells in patients with higher disease risk.

Dr Unwin added: “We next need to look at how mast cells are activated, and whether by preventing, or clearing mast cell activation we can slow or stop disease development.

“There are several researchers and companies looking at complement mediated-therapies for AMD and while these are promising for Chr1-related disease there is no evidence that they will have an effect on Chr10 disease.

“A therapy designed to target mast cell activation as a unified mechanism could in theory treat all patients with AMD and prevent sight loss “

Geraldine Hoad, the Macular Society’s research manager, said: “This is an exciting development and we look forward to seeing further research in this area. We know lots of current treatments for wet AMD don’t work for everyone and for those with dry AMD there is no treatment at all.  Finding something that works for everyone would be an important piece of the puzzle and make a huge difference to the lives of those affected.

“While this particular study is in its early stages. it’s great to see the benefit of our investment in the 51¸£ÀûÉç Eye Tissue Repository, which is proving a vital resource for lots of research in this area.â€�

The paper  Mast cell infiltration of the choroid and protease release are early events in age-related 2 macular degeneration associated with genetic risk at both chromosome 1q32 and 10q26 is published in

The Macular Society is the leading sight loss charity for people affected by macular disease. If you are affected by the conditions, or know someone contact the Society's Advice and Information Service on 0300 3030 111 or email help@macularsociety.org. Alternatively for more information on macular disease visit macularsociety.org

The breakthrough could one day herald the development of transformative treatments for developing age-related macular degeneration (AMD), which affects 600,000 people in the UK alone.

A test to determine which patients are at risk of developing the disease could also emerge, as the team estimate that 40-50% of patients have elevated levels of at least one of the five proteins, although more work still needs to be done.

The research, funded by Medical Research Council and a collaboration between scientists in 51¸£ÀûÉç, London and Tübingen in Germany, is published today (July 13th) in the American Journal of Human Genetics.

The discovery of new drug targets could help scientists develop therapies which lower levels of what are known as FHR proteins - and therefore the risk of developing or exacerbating AMD.

Scientists have long known that inflammation at the back of the eye plays a role in AMD development.

A series of genes thought to regulate the activity of the complement pathway – a key player in our immune defence against pathogens – were identified in previous research as candidates that affect a person’s risk of developing the disease.

However, until now the role of these genes – Complement Factor H (CFH) and Complement Factor H-Related 1 to 5 (CFHR-1 to CFHR-5) – has been unclear.

But by studying the levels of the products of these genes – FH and  FHR-1 to FHR-5 proteins– in 604 blood plasma samples using a method called mass spectrometry, the team was able to show for the first time that all five FHR proteins are at higher levels in people with AMD than in those without.

Part of the innate immune system, the complement pathway is our first line of defence against infections and clears damaged cells by marking them for destruction and recruiting and activating other immune cells.

In AMD, the complement pathway is over activated in the back of the eye, promoting an inappropriate and damaging inflammatory response.

Dr Richard Unwin from 51¸£ÀûÉç’s Stoller Biomarker Discovery Centre said: “This is a hugely important study for people with AMD. Measuring the levels of these FHR proteins has been a big challenge over the last few years and is technically quite challenging as they are present at low levels in the blood and are very similar to each other.

“By using state-of-the-art mass spectrometry methods we can now confidently measure these proteins and show for the first time what is an important, if not the most important, factor in how AMD develops.

“This opens up whole new areas for improving patient care, through the development of new treatments targeted at these proteins or in simply monitoring levels to discover who has higher levels of complement activation and as such will benefit from complement-modifying treatments.

“It’s important to stress that studies over time need to be carried out before we can say with authority that these proteins are able to predict risk – and that will take time.

“We’re confident about our results: a second study by Dr. Laura Lorés-Motta and Prof Anneke den Hollander at Radboud University in the Netherlands has in parallel arrived to the same conclusion about FHR proteins using a different measuring technique.”

In its early stages, AMD starts to damage the back of the eye forming deposits after which then patients go on to develop two form of the disease: wet or dry AMD. But the team hope that intervening at an early stage could stop its progression.

Dr Valentina Cipriani, a Lecturer in Statistical Genomics at Queen Mary University of London who led the data analysis said “For more than 15 years the focus for AMD has been on Complement Factor H and its protein FH. Our analysis clearly points beyond FH.”

“By using an approach called a genome-wide association study that looks at genetic variants across the genomes of people with and without the disease, we were able to identify genetic variants that determine both higher FHR protein levels and increased risk of AMD.”

Prof Simon Clark, Helmut Ecker Endowed Professor of AMD at Eberhard Karls University of Tübingen who co-supervised the work said “This really marks a step-change in our understanding around the driving mechanisms behind specific types of AMD.

“It follows on from our original discovery last year around FHR-4, but while all higher levels of at least one of the five FHR proteins are now known to be associated with AMD risk not all patients will have their disease driven by this route.

“Therefore, being able to measure these proteins in patients’ blood will be vital in identifying patients who will react to FHR-targeting therapies sometime in the future.”

Images demonstrate  what someone with AMD might experience

Between 1 and 1.4 million fungal eye infections occur in the developing world per year, leaving over 600,000 people blind in one eye, find researchers from 51¸£ÀûÉç, London and Nairobi.

Lead researcher Lottie Brown from the University of 51¸£ÀûÉç today publishes the first estimation of global fungal keratitis figures in

Infection of the transparent cornea of the eye can be devastating, especially if it is caused by fungal keratitis, say the team.

The infection - which often sets in after an agricultural accident - results in visual impairment, blindness and disfiguration. It can lead to discrimination, loss of employment and social isolation, reinforcing the cycle of poverty.

Outcomes of fungal keratitis cases, which are usually diagnosed too late to save vision, are poor: 60% of sufferers will go blind in the affected eye and 10% will need surgical removal of the eye. In contrast early diagnosis usually saves both vision and the eye, although a high level of expertise, antifungal therapy and often surgery is required.

The researchers identified high rates of fungal keratitis in a number of African countries as well as Nepal, Pakistan and India. Lower rates were identified in Europe.

of 51¸£ÀûÉç and Chief Executive of the (GAFFI) said: “Fungal keratitis is so neglected among neglected tropical diseases, even the WHO and G-Finder don’t list it. Poor agricultural workers are most affected, yet high quality care can takes days to access in most high incidence areas.

Professor Matthew Burton, practicing ophthalmologist at part of the London School of Hygiene &Tropical Medicine, declared: “Among all the major causes of eye infection in adults, fungal keratitis is too often devastating. My own experiences in Tanzania, Uganda, Nepal and India taught me what a challenge this problem can be – but enabled my team to develop pathways for major improvements in care.”

Lottie Brown, a final year medical student in 51¸£ÀûÉç, said: “Having seen these patients first hand in Nepal, I can testify to how awful fungal keratitis is. It has been a privilege to contribute to a better understanding of this ‘infectious accident’ which could affect anyone.”

The authors examined all 241 papers published listing the causes of microbial keratitis to derive country and regional estimates of annual incidence. In Kenya, Dr Michael Gichangi from the Ministry of Health had collected cases from each district over several years, enabling an estimate for Africa. The authors also checked for the ratio between fungal and bacterial keratitis which varied from 1% in Spain to 60% in Vietnam, typically ~45% in tropical and subtropical areas.

* rates are ~40% higher if culture and microscopy negative cases are assumed to be fungal.

The global incidence and diagnosis of fungal keratitis is publoshed in Lancet Infectious Diseases