Drug Database
TR

treprostinil

✓ Approved

United Therapeutics · PTGIR · Small Molecule

What is treprostinil?

treprostinil is a small molecule developed by United Therapeutics. It is approved for therapeutic indications via injectable (others) or subcutaneous injection.

Drug Profile

CompanyUnited Therapeutics
Drug ClassSmall Molecule
Molecular TargetPTGIR
RouteInjectable (Others), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, United Therapeutics

Mechanism of Action

Molecular Targets

treprostinil acts on 1 molecular target:

PTGIRprostaglandin I2 receptor (IP, PRIPR)
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Therapeutic Indications

treprostinil is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Respiratory, thoracic and mediastinal disordersPulmonary hypertension✓ Approved

Related Research Articles

PubMedJournal of controlled release : official journal of the Controlled Release Society2026-08-14

Formation of a pulmonary drug-depot by a double-ester treprostinil prodrug enables sustained lung-selective delivery.

Leone Giuditta G, Akoumia Kouame Kan Firmin KKF, Ucakar Bernard B, Esfahani Hrag H et al.

Prostacyclin analogues are effective treatments in pulmonary arterial hypertension (PAH), especially in advanced stages. Treprostinil, a stable prostacyclin analogue, can be administered as subcutaneous and intravenous infusions, oral extended-release tablets and inhalation. Inhalation offers several advantages over other routes of administration, including direct access to the lungs for localized therapy, reduced infection risk, and a painless, convenient mode of delivery. However, small lipophilic molecules like treprostinil are absorbed into the bloodstream within minutes after inhalation, resulting in a short duration of action in the lungs and systemic side effects. To address these limitations, we developed a novel strategy involving a double treprostinil prodrug tailored for pulmonary delivery. The prodrug consists of treprostinil di-esterified at its carboxylic acid with a polyethylene glycol (PEG) chain, and at its C11 hydroxyl group with butyric acid. The prodrug exhibited sustained treprostinil release in bronchoalveolar lavage fluid and serum, supporting its suitability for pulmonary delivery. It was cleaved by initial hydrolysis of the PEG chain, followed by subsequent cleavage of the short-chain fatty acid. Ex vivo studies in isolated pulmonary artery rings showed a delayed and prolonged vasorelaxation effect of the conjugate compared to the free drug. In vivo studies demonstrated significant lung retention, with detectable quantities of the compound remaining in the lungs 24 h after administration, and a markedly reduced peak serum concentration following inhalation. This double-prodrug approach represents a promising strategy for improving PAH treatment by optimizing local, sustained treprostinil delivery while minimizing systemic exposure.

PMID 42600698
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PubMedPulmonary circulation2026-08-14

Transitions From Parenteral Prostacyclin Analogues to Selexipag in Patients With Pulmonary Arterial Hypertension.

Kuebel Dalton J DJ, Collins Adele R AR, Jose Arun A, Guido Maria R MR et al.

Pulmonary arterial hypertension (PAH) is a progressive illness that may require therapy with parenteral prostacyclin pathway agents (PPA) (epoprostenol and treprostinil). These parenteral PPA's are continuous ambulatory infusions that require a high level of skill and knowledge to maintain safety and effectiveness. Depending on the clinical context, transition to oral prostacyclin receptor agonist therapy (selexipag) is sometimes pursued. To prevent abrupt withdrawal from parenteral PPA's, overlap transitions are typically used. This report describes 35 inpatient, rapid transitions from parenteral PPA's to oral selexipag. Planned hospital admissions for transition were common (n = 27, 77%), and all patients successfully transitioned without a return to parenteral PPA's in the immediate post-transition period. Most patients transitioned due to difficulties with current parenteral PPA therapy (n = 20, 57%), followed by an improved clinical status on parenteral PPA therapy (n = 8, 23%). The median length of transition was 36 h (IQR 24-48 h) and hospital stay was 3 days (IQR 2-6 days). Following transition, the cohort demonstrated stability in PAH-specific risk scores and functional status. All patients survived to outpatient pulmonary hypertension follow up (median 5.5 weeks, IQR 1.4-9.6 weeks), and the majority were alive at 1-year post-transition (n = 32, 91%). Based on these results, we conclude that transition from parenteral PPA's to selexipag can be done in the inpatient setting safely, quickly, and effectively.

PMID 42598408
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PubMedFrontiers in pharmacology2026-08-12

Exploring the therapeutic landscape of pulmonary hypertension associated with interstitial lung disease, with a focus on idiopathic pulmonary fibrosis: a narrative review.

Reccardini Nicolò N, Da Re Beatrice B, Mondini Lucrezia L, Salton Francesco F et al.

Pulmonary hypertension associated with idiopathic pulmonary fibrosis (PH-IPF) is a frequent and clinically relevant complication that worsens exercise capacity, quality of life, and survival. This narrative review summarizes the epidemiology, pathophysiology, diagnostic approach, and therapeutic landscape of PH-IPF. The development of PH in IPF reflects the combined effects of fibrotic parenchymal destruction, pulmonary vascular remodeling, hypoxic vasoconstriction, endothelial dysfunction, and altered vascular signaling. Diagnosis remains challenging because symptoms often overlap with those of advanced fibrotic lung disease and non-invasive tools have limited sensitivity; right heart catheterization remains the diagnostic gold standard. Antifibrotic agents are central to IPF management but have no established role as PH-targeted therapies. Most pulmonary arterial hypertension therapies have failed to show benefit in PH-IPF or have raised safety concerns, with ambrisentan and riociguat associated with harm. Inhaled treprostinil is currently the only approved therapy with randomized evidence of efficacy in PH associated with interstitial lung disease, including IPF. Supportive care, optimization of comorbidities, referral to expert centers, and timely lung transplantation evaluation remain essential components of management.

PMID 42582535
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PubMedJACC. Case reports2026-07-30

Pseudo-Infarction Reversal in Right Precordial Leads: ECG Evolution in Severe Pulmonary Hypertension.

Wang Lina L, Cui Yuxia Y, Song Jing J, Zhao Qinghao Q et al.

An acute pulmonary hypertension (PH) crisis causes dynamic electrocardiographic (ECG) changes, but complete post-therapy normalization-especially in post-transplant thrombotic microangiopathy (TMA) patients-is rarely documented. A 53-year-old man with acute myeloid leukemia after allogeneic hematopoietic stem cell transplantation presented with dyspnea. Right heart catheterization confirmed an acute pulmonary hypertension crisis (mean pulmonary arterial pressure: 52 mm Hg) secondary to thrombotic microangiopathy. Treatment with inhaled nitric oxide and treprostinil led to improvement. Follow-up echocardiography showed normalized pulmonary arterial pressure (35 mm Hg), resolution of ECG abnormalities (including a myocardial infarction pattern in the right precordial leads), and no PH recurrence. This case highlights TMA as a rare cause of reversible, vasoreactive PH after hematopoietic stem cell transplantation and documents the full ECG evolution during PH crisis and recovery. ECG monitoring is essential for diagnosing and tracking acute PH crises in transplant patients. Post-transplant TMA can cause reversible PH, requiring prompt hemodynamic assessment and targeted therapy.

PMID 42530193
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PubMedFrontiers in pharmacology2026-07-23

Pharmacovigilance assessment of gout: a real-world study using the FAERS database.

Ren Honghao H, Yao Nannan N, Ren Xiaodong X, Su Yani Y et al.

Drug intervention is a key method for preventing gout, various drugs have been implicated as potential risk factors in individual studies. This study aims to comprehensively identify drugs linked to the development of gout. Data were obtained from the FDA Adverse Event Reporting System (FAERS), and disproportionality analysis was employed to quantitatively assess the associations between drugs and gout. Four complementary signal detection methods-Reporting Odds Ratio (ROR), Proportional Reporting Ratio (PRR), Bayesian Confidence Propagation Neural Network (BCPNN), and Multi-item Gamma Poisson Shrinker (MGPS)-were utilized. To further delineate exposure-outcome relationships and identify influential predictors, least absolute shrinkage and selection operator (LASSO) logistic regression was implemented. Time-to-onset (TTO) analysis was conducted to examine the temporal dynamics between drug initiation and the occurrence of gout. Finally, a comprehensive assessment of the therapeutic indications of the drugs was performed. A total of 35 drugs were ultimately identified as potentially associated with the onset and progression of gout. Among these, several agents have been previously reported in the literature as having possible links to gout development. In addition, a number of novel candidates were detected for which evidence of an association with gout remains limited or has not been clearly established. These include Lenalidomide, Sacubitril valsartan, Ruxolitinib, Treprostinil, Octreotide, Selexipag, Rosuvastatin, Sitagliptin, Riociguat, Epoprostenol, Patiromer, Dasabuvir ombitasvir paritaprevir ritonavir, Tafamidis, Sparsentan, and Iloprost. Furthermore, TTO analysis suggested that approximately 75% of gout events occurred within 0.6 years following initiation of therapy. These pharmacotherapeutic agents are employed across diverse clinical settings, encompassing haematological malignancies, cardiovascular diseases, and pulmonary hypertension. These findings suggest the potential for targeted monitoring of drug-associated gout in clinical practice. When administering these medications, it may be crucial to regularly assess patients' uric acid levels and maintain heightened awareness for the possible onset of gout.

PMID 42488563
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PubMedMed (New York, N.Y.)2026-07-11

Inhaled treprostinil and the vascular turn in pulmonary fibrosis.

Yanagihara Toyoshi T, Kolb Martin M

TETON trials recently evaluated inhaled treprostinil in idiopathic pulmonary fibrosis (IPF) using two parallel phase 3 studies in different world regions. Both met the primary endpoint, demonstrating significantly less one-year forced vital capacity decline versus placebo. This viewpoint critically appraises the findings and contextualizes them within the evolving IPF treatment landscape.

PMID 42431188
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