Syncona Ltd (LON: SYNC), a leading healthcare company focused on founding, building and funding global leaders in life science, today announced that it has made a $80.0 million commitment in a Series C financing by Freeline. Syncona has funded the first tranche of this commitment, amounting to $40.0 million (£30.6 million)[3]. Syncona has a 79 per cent fully diluted ownership stake at the point full current commitments are invested.
· $80.0 million (£61.1 million)[1] commitment to Freeline in a Series C financing, a leading gene therapy company focused on liver expression for a range of chronic systemic diseases
· Freeline has a pipeline of four disclosed programmes, two of which are clinical stage, and is developing a next-generation gene therapy using a proprietary, novel capsid and best-in-class manufacturing platform
· Freeline is valued at cost[2] and held at £149.1 million following the first tranche of $40.0 million (£30.6 million) of the Series C investment
Freeline is progressing FLT180a, its lead programme in Haemophilia B, through clinical development. The company has reported that the first two patients in its ongoing Phase 1/2 trial who were treated with the lowest dose[4] have shown that Factor IX (FIX) activity remains stable and consistent at 40.5±4.5% through weeks 66 and 74 post administration. The normal range of FIX activity in the general population’s blood is between 50 per cent and 150 per cent. Freeline uses a novel capsid which is capable of driving high protein expression. The company continues to enrol Haemophilia B patients as part of its dose-ranging trial. Freeline is currently seeking to identify the optimal dosing regimen to deliver FIX activity consistently in the normal range for all patients and will report further data in this financial year (by March 2020).
Freeline has also recently dosed the first patient in its second programme in Fabry Disease, which it is estimated affects one in every 40,000[5] people. This programme is the first clinical stage AAV gene therapy study targeting Fabry Disease globally. The company also has disclosed pre-clinical programmes targeting Gaucher Disease and Haemophilia A, which are part of a broad pipeline of systemic disorders, where high protein expression is crucial to providing functional cures for patients.
Syncona’s first tranche of $40.0 million will enable the company to expand its team, continue to develop its robust manufacturing platform including commercial supply capability, generate further data in its clinical programmes for Haemophilia B and Fabry Disease and continue to progress its pipeline.
Chris Hollowood, Chief Investment Officer of Syncona ltd and Executive Chairman of Freeline, said:
“Freeline has developed a high-quality gene therapy platform with a novel capsid capable of driving high expression levels to treat systemic diseases. We are encouraged by the potential product profile in our lead programme in Haemophilia B and believe Freeline has the opportunity to achieve functional cures for patients across a broad pipeline of systemic diseases. We are continuing with dose optimisation and remain on track to provide a clinical data update by financial year end.
“This financing demonstrates Syncona’s differentiated approach of funding our companies over the long term. Our deep capital base enables us to continue to strongly back our companies as they progress through the development cycle and navigate clinical and operational risks. We look forward to continuing to work in close partnership with Freeline.”
In line with Syncona’s valuation policy, we continue to hold our investment in Freeline at cost[6] until material clinical data is generated, or a third-party financing or other factor occurs, that indicates that cost[7] is no longer the appropriate measure of fair value.
[1] As at exchange rate on 18 December 2019
[2] For the purposes of fair value, cost is equivalent to calibrated cost
[3] See footnote 1
[4] The first cohort were treated at 4.5x1011vg/kg
[5] http://www.fabry.org/fsig.nsf/pages/fabry
[6] See footnote 3
[7] See footnote 3
