Pharmachim S.A. announces an exclusive commercialization agreement with Purpose Pharma for diflunisal in Greece and Cyprus
Athens, June 1st, 2026 – Pharmachim S.A., today announced a strategic, exclusive agreement with Purpose Pharma International AB, a European rare disease biopharmaceutical company, for the commercialization of diflunisal in Greece and Cyprus. Under the terms of the agreement, Pharmachim will be exclusively responsible for the regulatory, medical, market access, and commercial activities for the therapy in these two countries.
Diflunisal has received marketing authorization from the European Commission as a treatment for hereditary transthyretin-mediated amyloidosis (hATTR) in adult patients with stage 1 and stage 2 polyneuropathy.[1] It is an oral therapy designed to stabilize the transthyretin (TTR) protein, slowing the progression of this debilitating and life-threatening rare disease.
Mr. Michael Tsatsaronis, CEO of Pharmachim S.A., stated:
"We are very pleased to announce our partnership with Purpose Pharma, a company that shares our deep commitment to addressing severe unmet medical needs. Hereditary ATTR amyloidosis is a devastating, progressive disease that deeply impacts patients and their families. This agreement allows us to leverage our extensive infrastructure and expertise in specialty medicines to ensure that eligible patients in Greece and Cyprus gain access to an effective, oral treatment option that can meaningfully delay disease progression."
Mr. Jonas Hansson, Chief Executive Officer of Purpose Pharma, noted:
"Following the European approval of diflunisal, our priority is to ensure that patients across Europe can benefit from this important therapy as swiftly as possible. Pharmachim’s proven track record in market access and commercialization within the Greek and Cypriot healthcare systems makes them the ideal strategic partner. We look forward to working closely together to bring this much-needed innovation to the local rare disease community."
About Hereditary Transthyretin-Mediated (hATTR) Amyloidosis
Hereditary transthyretin-mediated (hATTR) amyloidosis is a progressive and fatal genetic disease caused by mutations in the transthyretin (TTR) gene. The mutation destabilizes the TTR protein, causing it to misfold and form amyloid fibrils that accumulate in multiple organs, most notably the peripheral nerves, heart, and gastrointestinal tract. Patients suffering from stage 1 and stage 2 polyneuropathy experience progressive sensory loss, debilitating motor weakness, and a rapid decline in their ability to perform daily functions independently.
High Epidemiological Burden in Greece and Cyprus
While hATTR is classified as a rare disease globally, the Eastern Mediterranean represents a uniquely significant endemic cluster. Both Greece and Cyprus exhibit exceptionally high prevalence rates compared to the rest of Europe, placing a disproportionate burden on local healthcare systems and affected families.[2]
• Cyprus: The disease is highly endemic across the island, primarily driven by the Val30Met (also known as Val50Met) mutation. Cyprus reports a high national prevalence of approximately 3.72 cases per 100,000 people.[3] Patients in this region typically experience a highly aggressive disease course, with the debilitating onset of polyneuropathy symptoms frequently beginning around the age of 46.[3]
• Greece: The island of Crete has been clinically identified as having one of the highest hATTR frequencies worldwide, with an estimated prevalence exceeding 35 cases per 1 million inhabitants.[4] The Greek patient population demonstrates distinct genetic heterogeneity, predominantly harboring the Val50Met/Val30Met, Val114Ala, and Arg54Gly mutations.[4] These variants lead to severe, early-onset sensorimotor polyneuropathy, autonomic dysfunction, and restrictive cardiomyopathy.
Due to these dense, localized patient clusters, the introduction of a targeted, oral therapeutic option like diflunisal is of critical public health importance for the region, offering a much-needed intervention to preserve patient mobility and independence.
About Diflunisal
Diflunisal is an orally administered transthyretin stabilizer. It works by binding to the TTR protein, preventing its dissociation into amyloid-forming monomers and thereby halting the accumulation of toxic amyloid deposits.[5]
The European approval was based on a landmark, international, randomized, double-blind, placebo-controlled Phase 3 clinical trial involving 130 patients with hATTRexhibiting clinically detectable peripheral or autonomic neuropathy. Patients were randomly assigned to receive either 250 mg of diflunisal or a placebo twice daily for a period of two years.[6]
The trial successfully met its primary endpoint, demonstrating a statistically and clinically significant reduction in disease progression alongside the preservation of patient quality of life. Key clinical trial results demonstrated:
• Decelerated Neurological Impairment: Disease progression was measured using the Neuropathy Impairment Score plus 7 nerve tests (NIS+7), which ranges from 0 (no deficits) to 270. Over 24 months, the NIS+7 score worsened by 25.0 points in the placebo group, compared to an increase of only 8.7 points in the diflunisal group—a highly significant 16.3-point treatment difference (P < .001).[6]
• Preserved Quality of Life (QoL): Quality of life was measured using the 36-Item Short-Form Health Survey (SF-36). Patients treated with diflunisal showed stabilization or improvement in both physical and mental health.[7] Mean physical scores increased by 1.5 points with diflunisal (versus a 4.9-point decline in placebo, P < .001), while mental scores increased by 3.7 points (versus a 1.1-point decline in placebo, P = .02).[6]
About Pharmachim S.A.
Pharmachim S.A. is a leading pharmaceutical company based in Greece, specializing in the commercialization of innovative therapies and orphan drugs. By partnering with leading global biopharmaceutical organizations, Pharmachim utilizes its robust expertise in regulatory affairs, market access, and commercial execution to improve patient access to advanced specialty medicines across Greece and Cyprus. Pharmachim is a member of the Prime Group of companies.
About Purpose Pharma
Purpose Pharma International AB is a European pharmaceutical company that focuses on the development and commercialization of innovative products for rare diseases and specialty care areas characterized by high unmet medical need.
Media Contact:
Pharmachim S.A.
Phone: (+30) 210-5775475
Email: info@pharmachim.gr
www.pharmachim.gr
References
[1] European Medicines Agency. Attrogy (diflunisal): EPAR – Medicine overview. EMA/153788/2025. Marketing authorisation issued 17 July 2025. Available at: https://www.ema.europa.eu/en/medicines/human/EPAR/attrogy
[2] Parman Y, Adams D, Obici L, et al. Sixty years of transthyretin familial amyloid polyneuropathy (TTR-FAP) in Europe: where are we now? A European network approach to defining the epidemiology and management patterns for TTR-FAP. Curr Opin Neurol. 2016;29(Suppl 1):S3–S13. doi:10.1097/WCO.0000000000000288
[3] Dardiotis E, Koutsou P, Papanicolaou EZ, et al. Epidemiological, clinical and genetic study of familial amyloidotic polyneuropathy in Cyprus. Amyloid. 2009;16(1):32–37. doi:10.1080/13506120802676948
[4] Tzagournissakis M, Foukarakis E, Samonakis D, et al. High hereditary transthyretin-related amyloidosis prevalence in Crete: genetic heterogeneity and distinct phenotypes. Neurol Genet. 2022;8(5):e200013. doi:10.1212/NXG.0000000000200013
[5] Sekijima Y, Dendle MA, Kelly JW. Orally administered diflunisal stabilizes transthyretin against dissociation required for amyloidogenesis. Amyloid. 2006;13(4):236–249. doi:10.1080/13506120600960882
[6] Berk JL, Suhr OB, Obici L, et al. Repurposing diflunisal for familial amyloid polyneuropathy: a randomized clinical trial. JAMA. 2013;310(24):2658–2667. doi:10.1001/jama.2013.283815
[7] Sekijima Y, Tojo K, Morita H, Koyama J, Ikeda S. Safety and efficacy of long-term diflunisal administration in hereditary transthyretin (ATTR) amyloidosis. Amyloid. 2015;22(2):79–83. doi:10.3109/13506129.2014.997872