Press Release
Dec 14, 2021
Actimed Therapeutics Achieves Major Corporate Milestone – Initiation of first clinical study of new salt of S-pindolol (ACM-001.1)


  • Actimed Therapeutics initiates the company’s first clinical study of the pharmacokinetics and pharmacodynamics (PK/PD) for a new salt of S-pindolol (ACM-001.1)
  • This study is a prelude to the commencement of a Phase 2b clinical programme in patients
  • ACM-001.1 has the potential to become the first globally approved drug to treat cancer cachexia


London, UK – 14 December 2021. Actimed Therapeutics Ltd announces that following regulatory approval from the UK Regulatory Agency, it has commenced a clinical study in healthy subjects to evaluate the PK and PD of its lead compound, ACM-001.1, a new salt of S-pindolol that is under development as a treatment for cancer cachexia.

The study will be conducted in healthy subjects in two parts. It will compare ACM-001.1 to pindolol and will investigate both single and multiple dose PK and assess a range of doses of ACM-001.1.

Data from the study are expected in the first half of 2022 and will be used to inform the Phase 2b programme which is planned for late 2022.

Robin Bhattacherjee, Actimed CEO, commented: “This is an exciting time in the development of our new salt form of S-pindolol. We have worked hard on the development of this formulation over the last 2 years given the considerable benefits it delivers including improved stability, scalability for commercial manufacture and the potential for significantly extended patent life. The PK/PD study is a key clinical development milestone towards our ultimate aim of securing the first global approval for the treatment of cancer cachexia, a hugely under-served disease which is estimated to affect 50-80% of all cancer patients.”

About Actimed Therapeutics

Actimed Therapeutics is a clinical stage biopharmaceutical company focused on bringing innovation to the treatment of muscle wasting disorders to transform the care of an underserved and vulnerable patient population. Actimed was founded in 2017 by Stefan Anker and Andrew Coats, two world leading physicians in muscle wasting research.

The lead area of focus for Actimed is specifically in cachexia. Cachexia is a wasting disease that accompanies cancer and other serious chronic illnesses and is associated with significant morbidity and mortality. Despite its prevalence and devastating clinical effects, there is no globally approved drug for the treatment or prevention of cancer-related cachexia.

It has been estimated that cachexia affects 50–80% of cancer patients and accounts for up to 20% of cancer deaths. Treating cancer cachexia successfully may increase both the length and quality of life for cancer patients1.

The lead product of Actimed, S-pindolol (ACM-001.1), is an anabolic/catabolic transforming agent2 (ACTA). In nonclinical models, S-pindolol has been shown to target multiple pathways that drive cachexia and has generated promising proof of concept Phase II clinical data in cachexia patients3. Actimed is currently preparing for further clinical studies in cachexia in Non-Small Cell Lung Cancer (NSCLC) and Colorectal Cancer (CRC).

Actimed has licensed the global rights to develop and commercialise S-oxprenolol, the Company’s second product, for cancer cachexia and any other indications outside of amyotrophic lateral sclerosis (ALS) to Faraday Pharmaceuticals. Actimed retains global rights to S-oxprenolol in ALS, where loss of body mass and muscle wasting may impact survival.

1 Argiles JM, Busquets S, Stemmler B, Lopez-Soriano FJ. Cancer cachexia: understanding the molecular basis. Nat Rev Cancer. 2014;14:754–62.
2 Pötsch MS, et al. The anabolic catabolic transforming agent (ACTA) espindolol increases muscle mass and decreases fat mass in old rats. J Cachexia Sarcopenia Muscle. 2014 Jun;5(2):149-58
3 Coats AJS, et al. Espindolol for the treatment and prevention of cachexia: a randomized, double‐blind, placebo‐controlled, international multicentre phase II study (the ACT‐ONE trial). J Cachexia Sarcopenia Muscle 2016 Jun; 7(3):355-365.