Nuformix plc (LON:NFX), a pharmaceutical development company targeting unmet medical needs in fibrosis and oncology via drug repurposing, has announced its unaudited results for the six months ended 31 March 2026.
Operational highlights
· The Board continues to believe that NXP002, Nuformix’s lead programme, offers a potentially significant treatment for progressive fibrosing interstitial lung diseases (ILDs), including Idiopathic Pulmonary Fibrosis (IPF) and Progressive Pulmonary Fibrosis (PPF), and is focused on generating data and further progressing on-going discussions with potential partners that is expected to support its efforts to secure a licensing, option or collaborative agreement for NXP002.
· During the period the Company announced that the U.S. Food and Drug Administration (FDA) had granted Orphan Drug Designation (ODD) in IPF for tranilast lystate, the active drug substance enabled for inhaled delivery in NXP002.
Financial Highlights
· Loss on ordinary activities (after tax credit) of £346,577 (31 March 2025: loss of £376,668)
· Loss per share 0.02p (31 March 2025: 0.03p)
· Net assets of £1,636,439 (31 March 2025: £807,653) including £930,283 of cash and cash equivalents at 31 March 2026 (31 March 2025: £97,911)
· In November 2025, an oversubscribed open offer raised gross proceeds of £228,081 through the issue of 114,050,535 new ordinary shares at a price of 0.2 pence per share.
· In March 2026, a subscription for 500,000,000 new ordinary shares at a price of 0.2 pence per share raised gross proceeds of £1,000,000.
Dr Dan Gooding, Executive Director of Nuformix, said: “Our on-going research efforts and progressive external discussions to date validate that inhaled treatment of IPF and related fibrotic lung diseases via NXP002 remains a viable and attractive concept. In March 2026 we were delighted to receive news of the FDA’s award of Orphan Drug Designation in IPF for NXP002. Given the EMA’s award of the same, these achievements support the plausibility of our differentiated approach, targeting fibrosis resolution and restoration of tissue function, whilst allowing healthy repair, which has been very helpful in advancing partnering discussions. The March placing proceeds are allowing us to generate value-enhancing data and progress the NXP002 programme, aligning with feedback from potential partners and supporting our focussed efforts to secure an out-licensing partner for NXP002. I remain excited by our future prospects and look forward to providing further updates in due course as appropriate.”
Chairman’s statement
Operational review
NXP002 is the Group’s lead asset and a potential novel inhaled treatment for Idiopathic Pulmonary Fibrosis (“IPF”), Progressive Pulmonary Fibrosis (“PPF”), and other progressive fibrosing interstitial lung diseases (“ILD”). NXP002 is a proprietary, new form of the drug tranilast with enhanced physical properties that allow delivery direct to the lung via nebulisation.
There are more than 200 types of ILD, which are characterised by varied amounts of inflammation, scarring, or both, that damage the lung’s ability to absorb oxygen. IPF is the most well-known form of ILD, affecting approximately 100,000 patients per year in the US. PPF previously referred to as Progressive Fibrosing ILD (PF-ILD), is a larger and even more poorly served segment of the ILD market, affecting approximately 200,000 patients per year in the US.
IPF and PPF are devastating lung diseases associated with a higher mortality rate than many cancers with median survival of 3 to 5 years. Thus, IPF and PPF represent a high unmet medical need such that the requirement for improved treatment options represents what the Directors believe to be a significant commercial opportunity. IPF is classified as a rare disease and presents a global commercial market that is forecast to grow to US$6.4bn by 2031. Sales of standard-of-care (“SoC”) therapy OFEV achieved EUR3.8bn in 2024. Sales of Esbriet, also an IPF SoC therapy peaked in 2020 at USD1.2bn prior to genericisation.
Tranilast has a long history of safe use as an oral drug for asthma, keloids and hypertrophic scarring, but while there is growing evidence that supports its potential use in other fibrotic conditions, including IPF, a combination of poor physicochemical properties, variable pharmacokinetics and challenging pharmacodynamics following oral delivery limit its potential use in ILDs. NXP002 is differentiated as it is a patent protected, novel form of tranilast that has been optimised for formulation and delivery direct to the lungs by inhalation, potentially overcoming the issues using tranilast orally as a chronic treatment for fibrosing ILDs.
The inhalation route is a well-known delivery strategy for the treatment of lung diseases to yield greater efficacy and reduce systemic, off-target side-effects compared to oral treatment. Discontinuation of treatment in IPF and PPF patients is currently an issue in the treatment of these diseases with discontinuation rates for current SoCs up to 80% in certain patient groups due to, in part, their debilitating systemic side effects. The Directors believe effective inhalation therapies offer the potential to overcome these limitations of oral therapies.
The positioning of NXP002 as an inhaled treatment for IPF and PPF could be either as added to SoC treatments or administered as a monotherapy for patients non-responsive to SoCs and those declining these therapies due to side effects which significantly impact their quality of life.
The preclinical inhalation strategy, initiated by the Company, has significantly progressed NXP002 demonstrating:
| · | drug can be delivered in-vivo by a range of nebulisers at the optimum droplet size for delivery to the deep lung; |
| · | very high doses of drug appear to be well-tolerated; and |
| · | an in-vivo inhalation dose response was observed across both inflammation and fibrosis biomarkers that is consistent with all ex-vivo human IPF tissue studies to date. |
The Company conducted studies in a new iteration of a 3D human IPF lung tissue model, that has been advanced to significantly reduce output variability, offering greater disease and species relevance. The results for NXP002 alone and in combination with current SoC’s, can be summarised as follows:
| · | NXP002 is well tolerated in ex-vivo human lung tissue with no signs of toxicity events; |
| · | NXP002 alone delivers a strong, consistent anti-fibrotic and anti-inflammatory effect as demonstrated by modulation of the release of multiple biomarkers of fibrosis and inflammation; |
| · | both high and low concentrations of NXP002 show an additive anti-fibrotic and anti-inflammatory effect to SoC; |
| · | in particular, the higher concentrations of NXP002 with SoC’s deliver a near complete ablation of fibrosis biomarker release, yet at lower concentrations than have been seen in other preclinical models to date; and |
| · | the clear, pronounced additive benefit of NXP002 on top of SoCs observed suggests that NXP002 will provide additional efficacy, even in patients responding to SoC therapy. |
This raises the possibility that NXP002 targets additional disease pathways to SoC’s when increasing the combined anti-fibrotic and anti-inflammatory response. Following success in suppressing biomarkers of fibrotic disease progression in human IPF lung tissue, the same samples were analysed to assess additional mechanistic and anti-inflammatory benefits on top of SoC’s and the results are summarised as follows:
| · | NXP002 alone delivers a strong, consistent anti-inflammatory effect as demonstrated by suppression of the release of inflammatory cytokines by over 90% for all cytokines studied; and |
| · | the results further suggest that NXP002 may provide additional efficacy in combination with SoC’s, even in patients not responding to SoC therapy alone. |
Nuformix has developed a Target Product Profile (TPP) that is consistent with twice daily inhalation administration. To assess NXP002’s duration of action in relation to the TTP, the Company initiated work in an exploratory model using healthy human lung tissue. The model also bridges the Company’s successful preclinical work across a variety of LPS-challenge studies. The results are summarised as follows:
| · | NXP002 suppresses the release of inflammatory cytokines by healthy human lung tissue following LPS challenge; and |
| · | a strong anti-inflammatory effect remains at 12 hours post drug dosing demonstrated by continued suppression of the release of inflammatory cytokines following LPS challenge, confirming NXP002 has a suitable duration of action to support its TTP of twice daily dosing. |
Data from the precision-cut lung slice (“PCLS”) disease model referred to above using lung tissue from IPF patients were reanalysed as part of on-going discussions with potential licensing and development partners for NXP002. NXP002 had also been studied in tissue from an autoimmune ILD explanted lung (in this case from a patient diagnosed with non-specific interstitial pneumonia or NSIP). This collective data was revisited to compare key biomarker changes in tissue in response to NXP002 treatment using an ‘area under the curve’ (AUC) based approach, considering total biomarker expression during the treatment period. These new results are summarised as follows:
| · | a clear dose response to NXP002 was observed across both extra cellular matrix (“ECM”) biomarkers and pro-fibrotic mediators suggesting NXP002’s activity in additional pathways to standards of care; |
| · | a consistent and significant effect of NXP002 was observed alone and in combination with standards of care across both biomarker types in all donors; |
| · | when the Col1A1 gene was found to be overexpressed in tissue, representing active fibrotic disease and tissue turner, NXP002 consistently attenuates its expression. When Col1A1 is not overexpressed Col1A1 is maintained, which may point towards NXP002’s role in ECM homeostasis and supporting healthy tissue repair and regeneration, consistent with the evidence base describing positive results from clinical studies of tranilast in a range of fibrotic diseases; and |
| · | the autoimmune-ILD donor studied also showed a significant response across both biomarker types alongside the seven IPF donors confirming that NXP002’s activity translates well to autoimmune-derived ILDs. |
Nuformix has developed new insights relating to its NXP002 lead programme. Following an in-depth pharmacology review, leveraging human and AI-methodologies, the pathways associated with disease progression in fibrotic diseases in which NXP002 has demonstrated both activity and clinical translation have been assessed across multiple organs. The resulting outputs allow clear demonstration of NXP002’s potential to regulate four specific pathways that drive fibrotic disease. This includes core pathways, such as the TGF- ß pathway, but also evidences regulation of the WNT/ß-catenin and NLRP3 pathways, which are emerging as key disease progression pathways requiring suppression. The outputs also illustrate consistent translation from cell-based studies to clinical studies across multiple fibrotic organs, including the lung, in the resolution of extra cellular matrix deposition.
The Directors concluded that NXP002 as a potential treatment for IPF, was a likely candidate for Orphan Drug Designation (ODD), which could provide additional product protection against potential future competitors in addition to product development advantages.
On 10 March 2026 the Group announced that the FDA had granted ODD in IPF for tranilast lystate, the active drug substance enabled for inhaled delivery in NXP002. The FDA grants ODD for investigational treatments for rare diseases, such as IPF, defined as affecting fewer than 200,000 people in the United States. ODD qualifies the developer for certain incentives with the goal of accelerating drug development for patients, including tax credits for clinical trials or qualified clinical testing costs, a waiver of the Prescription Drug User Fee Act application fee when a marketing application is submitted, and the potential to receive seven years of marketing exclusivity upon product approval.
This follows the European Medicines Agency’s (“EMA”) decision to grant ODD in IPF for tranilast to the Group on 29 May 2025.
The Board continues to believe NXP002 offers a potentially significant treatment of progressive fibrosing ILDs, including IPF and PPF, and is focused on generating further data and progressing ongoing discussions with potential partners that may support its efforts to secure a licensing, option or collaborative agreement for NXP002. As a consequence, the following activities are being prioritised:
| · Continued investment into maintenance and prosecution of key NXP002 IP; |
| · Continued work with industry experts and key opinion leaders to create a data package support programme progression and business development activities; |
| · Progression of partnering discussions with multiple parties with the aim of securing a licencing, option or collaborative agreement. |
Outlook
The Company continues to advance and exploit the current assets within the portfolio through the R&D and business development activities as set out above.
The strategy of the Group is to continue to increase the value of its existing assets while maintaining tight control of costs, including conducting business development/licensing activities using a structured and data-driven approach, with the goal of seeking global licensing deals.
Financial Review
In the first half of the financial year, the Board has focused its expenditure on R&D activities, such as the application to the U.S. Food and Drug Administration (FDA), and subsequent achievement of Orphan Drug Designation, that add value to the current assets while optimising the operation to minimise administrative expenditure and the operational cost-base.
Dr Julian Gilbert
Non-Executive Chairman
28th May 2026
