(AIM: SAR)

26 October 2015

Sareum Holdings plc

(“Sareum” or “the Company”)

Final Results

Sareum Holdings plc (AIM: SAR), the specialist cancer drug discovery and development business, is pleased to announce its final results for the year ended 30 June 2015.

Operational Highlights

• Final preparations to submit CHK1 candidate for two concurrent Phase 1 clinical trials to assess different administration strategies: one as a single agent and the other in combination with chemotherapy.
• CHK1 clinical trial applications expected to be submitted in Q1 2016 with trials to commence, subject to approval, shortly thereafter.
• Preclinical development of Aurora+FLT3 inhibitor progressing to plan, with toxicology and additional efficacy studies ongoing.
• TYK2 inhibitor lead molecule demonstrates striking decrease in psoriasis pathology in a disease model and encouraging results in a rheumatoid arthritis model.

Financial Highlights

• Net assets at period end were £1.86 million (2014: £1.72 million) of which £1.48 million comprised of cash at bank.

• Loss on ordinary activities (after tax credit) of £1,255,368 (2014: Loss of £763,000), an improvement on expectations, reflecting re-phasing of commitments to CHK1 programme.
• Successful placing in June 2015 to raise £1.44 million (before expenses) to satisfy ongoing commitments to CHK1 co-development payments and to provide additional working capital.

Dr Tim Mitchell, Chief Executive Officer of the Company, said:

“Good progress has been made in the last year, with two cancer programmes advancing through preclinical validation and potential new indications for our autoimmune disease programme. With the two planned in-human clinical trials for CHK1 commencing in early 2016, as well as the progress in our other programmes adding further commercial value, we look forward to next year with real anticipation and optimism.”

 

Enquiries:

Sareum Holdings plc
Tim Mitchell, Chief Executive Officer	01223 497 700
WH Ireland Limited (Nominated Adviser)
Chris Fielding / Nick Prowting	020 7220 1650
Hybridan LLP (Broker)
Claire Noyce / William Lynne	020 3764 2341
The Communications Portfolio (Media enquiries)
Ariane Comstive Ariane.comstive@communications-portfolio.co.uk	07785 922 354

 

Chairman and CEO's Statement

This year, in line with our stated strategy, we have concentrated on advancing our three lead drug discovery programmes in order to maximise their value and make them attractive to potential licensors and commercial partners.

The CHK1 programme, in collaboration with CRT Pioneer Fund, is in its final preparations before submitting the Clinical Trial Applications for Phase 1 clinical trials.  With positive preclinical results for the candidate both as a single agent and in combination with chemotherapy, two clinical trials applications are now expected be made in Q1 2016 and, if successful, trials should commence shortly thereafter.

We continue to make good progress with our TYK2 programme targeting autoimmune diseases, including psoriasis and rheumatoid arthritis.  Further investigations, funded in part by the Innovate UK Biomedical Catalyst, will also be conducted on the efficacy of our lead molecules against certain cancers that require TYK2 signalling for survival.  

Meanwhile, preclinical development of the Aurora+FLT3 candidate, with our Chinese partner HMUBEC (Hebei Medical University Biomedical Engineering Center), is progressing as planned. 

In addition to progressing these programmes towards in-human clinical trials, we have continued our work in securing the intellectual property that protects them.  Our SKIL platform is the foundation of our Aurora+FLT3 and TYK2 discoveries, and has the potential to produce inhibitors against many additional kinase targets. Patents for inventions associated with the platform have now been granted in the US, China and Japan, and we are currently awaiting confirmation for a European patent grant.  European and US patents have also been secured for our most advanced programme, CHK1, and more recently European and US patent grants for Aurora+FLT3, and a European grant for TYK2.

Further work is being undertaken to bring our programmes to the attention of the scientific community, including potential licence partners and investors, through publication in peer-reviewed journals and presentations at conferences and investor meetings.  In October 2014 the effect of SAR-20347, one of our TYK2 inhibitor molecules, on significantly reducing psoriasis pathology was described in the Journal of Immunology.  In July this year, the first description of an orally active clinical development candidate CHK1 inhibitor was made with the publication in the journal, Oncotarget, of how CCT245737 boosts the effectiveness of chemotherapies used to treat lung and pancreatic cancers. 

Financial review

The Company ended the year with net assets of £1.86 million (2014: £1.72 million) of which £1.48 million (2014: £701,000) comprised of cash at bank.

The loss after taxation for the year was £1.26 million (2014: loss of £763,000) reflecting the financial commitment of £497,000 made to the CHK1 programme during the course of the year as well as additional research funding invested in our TYK2 programme.

In June 2015, the Company raised £1.44 million (before expenses) via a share placing primarily to satisfy its ongoing commitment towards the co-development partnership for the CHK1 programme as we plan for its first in-human trials. A portion of the funds will also be used to provide additional working capital and research funding, particularly to progress our TYK2 autoimmune and inflammatory diseases programme.

Research Update

Checkpoint Kinase 1 (CHK1)

This is the most advanced programme in our pipeline. It is being developed in collaboration with CRT Pioneer Fund, and is now being prepared for clinical trials applications.

 

In preclinical studies, CCT245737, the clinical development candidate, has shown potent efficacy against various cancers when dosed, via the oral route, as a single agent as well as in combination with chemotherapies.  These cancers include lung, colon and pancreatic, as well as certain types of Acute Myeloid Leukaemia (AML), neuroblastoma and B-cell lymphoma. We believe this molecule has the potential to be a best-in-class compound.  In order to assess a fuller range of potential applications and therefore maximise the commercial value of the programme, two clinical trials are planned. The primary objectives of these trials are to assess the safety of CCT245737 and to determine dose levels for future studies. One trial plans to examine CCT245737 in combination with other chemotherapies, ultimately targeting lung and pancreatic cancers, and the second clinical trial plans to assess CCT245737 as a single agent in various cancer types.

 

Analysis of clinical trial data is greatly facilitated by the ability to monitor the extent of enzyme target inhibition that results from the administration of the candidate drug to patients. To this end, working with colleagues at the Institute of Cancer Research, the collaboration has developed a novel “biomarker” assay that quantitatively measures the degree of CHK1 inhibition by CCT245737. This biomarker assay is expected to translate into the clinical setting to confirm that CHK1 inhibition has occurred upon administering CCT245737.

 

These preclinical studies are on-track to complete in Q4 2015, as stated in our February 2015 Research Update. In our February 2015 Half-Yearly Results Statement, it was noted that application for clinical trials would be submitted within the same period. The additional data and administration required to support the plan for two Clinical Trials Applications means we now intend to submit these applications as early as possible in Q1 2016.

A financial commitment from Sareum of £797,500 will be triggered one month before the Clinical Trials Applications and this payment is expected to be made around the end of this calendar year.

Aurora+FLT3

In collaboration with our Chinese partner, HMUBEC, we are now able to manufacture the larger scale batches of our preclinical development candidate that would be required for Phase 1 clinical trials.  We are now embarking on additional efficacy and toxicology studies which we expect to complete before our financial year end and, if successful, to file clinical trials applications in multiple territories shortly thereafter.

In an in vivo disease model of AML, the candidate molecule demonstrates greater than 98% tumour inhibition. Patients with AML are susceptible to the development of resistance to current drugs used to treat their disease and, whilst our clinical strategy is still evolving, it is likely that such resistant patients will be a focus of any Phase 1 trial.  The molecule also has potent cell-killing activity against other cancers, particularly Acute Lymphoblastic Leukaemia (ALL), neuroblastoma and Anaplastic Large-Cell Lymphoma.

Alongside this preclinical development of the compound intended for intravenous dosing, good progress has been made in developing a new formulation that can be used to administer the candidate molecule via the oral route.  One formulation has been developed which we believe can deliver therapeutically useful amounts of the candidate when dosed orally. We have now begun assessment of efficacy and safety in a suitable disease model.

TYK2

TYK2 – Autoimmune and inflammatory disorders

Our autoimmune and inflammatory disorders programme, with co-development partner SRI International, is developing a series of orally bioavailable inhibitors of TYK2, a member of the Janus kinase (“JAK”) family of kinases. JAK family kinases are the targets of several marketed and clinical-stage drugs for cancer and autoimmune diseases, although none of these specifically target TYK2, giving us a potentially unique position in this area. 

We have previously reported the discovery of our initial lead candidate SAR-20347, which has shown that, when dosed via the oral route, it can significantly decrease psoriasis pathology in a disease model. Furthermore, we are pleased to report here that we have subsequently demonstrated an equally striking effect in a standard model of rheumatoid arthritis. In this model, SAR-20347 reduces joint inflammation in a dose-dependent manner, and is more effective than a commonly-used steroid treatment.

Recently synthesised analogues of SAR-20347 show improved potency against TYK2 and selectivity profiles against other JAK family kinases. We are currently assessing their pharmacokinetic properties before progressing into additional disease models such as ulcerative colitis.  

TYK2 – Cancer

Reports in the scientific literature have identified TYK2 inhibition as a potential strategy to directly target the growth of certain cancers, or to overcome resistance to targeted drugs in the treatment of certain cancers.  Cancers potentially requiring TYK2 signalling to spread or to develop resistance include small cell lung cancer, bone cancers and T-ALL, a type of leukaemia that predominantly affects children and adolescents.

In order to determine the feasibility of this novel approach we successfully secured a grant of £140K from the Innovate UK Biomedical Catalyst Fund to investigate the potential of our lead molecules to treat T-ALL.  This grant-supported project began in August 2015 and is expected to run for one year. 

Given the wide potential for our TYK2 programme we continue to seek a commercial research partner to sponsor the ongoing research with a view to licensing the programme at a later stage of development.

Outlook

We are extremely pleased that the CHK1 programme will have, subject to receiving clinical trials approval, two opportunities to demonstrate its potential.

With our CHK1 programme reaching a pivotal point early next year, and our other two advanced programmes progressing we continue to seek licence partners for these programmes as well as opportunities for further programme development.

Dr Paul Harper                                                                                                                                          Dr Tim Mitchell
Chairman                                                                                                                                     Chief Executive Officer

Annual Results 2015 available as PDF document: Annual Results 2015