We are a clinical-stage biopharmaceutical company focused on developing medicines for the treatment of hypertension and other cardiovascular diseases. Our product candidate, RTN-001, is a next-generation, once-daily, oral, small molecule phosphodiesterase-5 (“PDE-5”) inhibitor designed to reduce blood pressure by potentiating nitric oxide signaling, a key mechanism underlying the development and severity of hypertension. While first-generation PDE-5 inhibitors, such as Viagra (sildenafil), were originally studied in cardiovascular indications such as hypertension and angina, we believe they did not have adequate bioavailability and tissue penetration to impact the smooth muscle cells of the central vascular and cardiac tissues and thus failed to achieve clinically meaningful reductions in blood pressure. RTN-001 differs from first-generation PDE-5 inhibitors as it has been specifically engineered to have increased bioavailability and an increased distribution to the muscular arteries in the body such as the aorta and its branches in the central vasculature. In two Phase 2 pilot trials, RTN-001 achieved clinically meaningful placebo-adjusted reductions in systolic blood pressure (“SBP”) and diastolic blood pressure (“DBP”) in patients with hypertension and was generally well tolerated, with no drug-related serious adverse events (“SAEs”) reported. We believe RTN-001 has the potential to be an effective treatment for hypertension with a favorable safety profile and thus be part of an anti-hypertensive treatment approach. Hypertension is among the most prevalent chronic diseases worldwide and is a leading modifiable risk factor for preventable cardiovascular morbidity and mortality. Even small blood pressure reductions, as low as 5 mmHg, yield measurable improvements in major cardiovascular events and outcomes. Currently, we are developing RTN-001 for the treatment of patients with uncontrolled hypertension (“uHTN”), defined as individuals with blood pressure of 130/80 mmHg or higher while receiving two or more concomitant anti-hypertensive medications; and resistant hypertension (“rHTN”), defined as individuals whose blood pressure does not fall below 130/80 mmHg despite treatment with three or more agents, including a diuretic. In the United States, an estimated 120 million adults, or nearly half of all adults, have hypertension. Because severe hypertension is oftentimes asymptomatic, it is often described by physicians as “the silent killer”. Patients can be either unaware of the severity of their condition or have difficulty remaining compliant with the requisite polypharmacy necessary to control the disease. Persistent elevation of blood pressure is strongly associated with an increased risk of serious clinical consequences, including cardiovascular disease, heart failure, stroke, progressive renal impairment, and other end-organ damage, particularly in patients with other risk factors such as diabetes, obesity and aging. Notwithstanding the broad availability of various antihypertensive therapies, a substantial unmet medical need persists. RTN-001 was designed to lower blood pressure by enhancing nitric oxide signaling via the nitric oxide-cyclic guanosine monophosphate (“cGMP”) pathway. Nitric oxide is an endogenous vasodilator that directly dilates blood vessels via cGMP activation. Thus, the nitric oxide pathway is a critical component of blood pressure regulation by modulating the level of vascular tone, the degree of contraction of the arterial smooth muscle cells, the major cellular component of the muscular arteries comprising the central vasculature and its branches. PDE-5 is an enzyme that degrades cGMP. By inhibiting cGMP degradation, endogenous nitric oxide-mediated vasoregulatory mechanisms are enhanced. Nitric oxide is also a potent anti-inflammatory molecule, critical for reducing metabolic stress that occurs during the aging process, as well as in medical conditions associated with hypertension such as diabetes, hyperlipidemia and obesity. Enhancing PDE-5 inhibitor-mediated vasodilation is a well-established therapeutic mechanism in penile and pulmonary vasculature tissues, as thinner readily accessible vasculature is involved. As such, first-generation PDE-5 inhibitors are approved for use to treat erectile dysfunction (“ED”) and Type 1 Pulmonary Arterial Hypertension (“PAH”). Notably, first-generation PDE-5 inhibitors were unable to meaningfully reduce blood pressure, which we hypothesize is due to limited biodistribution into the thicker, more compartmentalized, and smooth muscle cell-rich central vascular tissues. RTN-001 was engineered using a proprietary surface chemistry-based platform that enables precise tuning of physicochemical properties to more effectively distribute into cardiovascular smooth muscle tissues than first-generation PDE-5 inhibitors. In October 2025, we initiated a randomized, multicenter, double-blind, placebo-controlled Phase 2b dose-ranging trial to: (i) identify the minimally effective and optimal dose of the modified release formulation of RTN-001 and (ii) assess the safety and efficacy of RTN-001 for the treatment of adult patients with uHTN while still under treatment with two to five concomitant antihypertensive medications in larger, “real world” settings. The primary endpoint of the trial is the change in peripheral office-seated SBP at week 4 compared to placebo. Key secondary endpoints of the trial include (1) mean change from baseline ambulatory blood pressure monitoring (“ABPM”) over 24 hours and (2) mean change in central blood pressure compared to placebo. Additionally, the trial includes pharmacokinetics and safety assessments to characterize drug exposure, support dose selection and evaluate the overall safety and tolerability profile of RTN-001. Exploratory endpoints include the assessment of the effect of RTN-001 on renal function and nocturnal hypertension. We believe this trial will enable and inform our planned Phase 3 clinical trial. Initial data is expected in the first half of 2027. Retension Pharmaceuticals, Inc. was incorporated as a Delaware corporation on July 26, 2023. Our principal executive office is in Falls Church, Virginia.
