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Interleukin-1 blockade with RPH-104 in patients with acute ST-elevation myocardial infarction: study design and
M Samsonov1, V Bogin2, B W Van Tassell3
1R-Pharm JSC, Moscow, Russia.
Insights
This study investigates RPH-104
Area of Science:
- Cardiology
- Immunology
- Pharmacology
Background:
- ST-segment elevation myocardial infarction (STEMI) triggers significant inflammation, increasing risks of mortality and heart failure (HF).
- Interleukin-1 (IL-1), a key inflammatory mediator, exacerbates myocardial damage post-STEMI.
- RPH-104 targets both alpha and beta isoforms of IL-1, potentially mitigating inflammatory responses.
Purpose of the Study:
- To evaluate the efficacy of RPH-104 in reducing inflammation and adverse outcomes following STEMI.
- To assess the impact of RPH-104 on high-sensitivity C-reactive protein (hsCRP) levels, a marker of inflammation.
- To determine the effect of RPH-104 on heart failure incidence, mortality, and cardiac function.
Main Methods:
- A double-blind, randomized, placebo-controlled trial involving 102 STEMI patients.
- Participants received a single dose of RPH-104 (80 mg or 160 mg) or placebo.
- Primary endpoint: hsCRP area under the curve (AUC) from day 1 to day 14; secondary endpoints include clinical outcomes and echocardiographic parameters over 12 months.
Main Results:
- The primary endpoint data (hsCRP AUC) is currently being collected.
- Secondary endpoint data collection includes mortality, heart failure hospitalizations, and cardiac function assessments.
- Study completion is anticipated in 2Q 2022, with results pending.
Conclusions:
- The study aims to establish RPH-104 as a novel therapeutic agent for STEMI.
- Findings will elucidate the role of IL-1 inhibition in managing STEMI complications.
- Results are expected to inform future clinical practice for STEMI management.
Background:
Myocardial injury of ST-segment elevation myocardial infarction (STEMI) initiates an intense inflammatory response that contributes to further damage and is a predictor of increased risk of death or heart failure (HF). Interleukin-1 (IL-1) is a key mediator of local and systemic inflammatory response to myocardial damage. We postulate that the use of the drug RPH-104, which selectively binds and inactivates both α and β isoforms of IL-1 will lead to a decrease in the severity of the inflammatory response which will be reflected by decrease in the concentration of hsCRP, as well as the rate of fatal outcomes, frequency of new cases of HF, changes in levels of brain natriuretic peptide (BNP) and changes in structural and functional echocardiographic parameters.
Methods:
This is a double blind, randomized, placebo-controlled study in which 102 patients with STEMI will receive a single administration of RPH-104 80 mg, RPH-104 160 mg or placebo (1:1:1). The primary endpoint will be hsCRP area under curve (AUC) from day 1 until day 14. Secondary endpoints will include hsCRP AUC from day 1 until day 28, rate of fatal outcomes, hospitalizations due to HF and other cardiac and non-cardiac reasons during 12-month follow-up period, frequency of new cases of HF, changes in levels of brain natriuretic peptide (BNP, NT-pro-BNP), changes in structural and functional echocardiographic parameters during 12-month follow-up period compared to baseline. The study started in October 2020 and is anticipated to end in 2Q 2022.
Trial Registration:
ClinicalTrials.gov, NCT04463251. Registered on July 9, 2020.
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