Drug Database
IL

iloprost (CiVi 030 / CIVI030 / Civi 030)

✓ Approved

SERB Pharmaceuticals · PTGIR · Small Molecule

What is iloprost?

iloprost is a small molecule developed by SERB Pharmaceuticals. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

Brand NamesCiVi 030, CIVI030, Civi 030
CompanySERB Pharmaceuticals
Drug ClassSmall Molecule
Molecular TargetPTGIR
RouteInjectable (Others), Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, SERB Pharmaceuticals

Mechanism of Action

Molecular Targets

iloprost acts on 1 molecular target:

PTGIRprostaglandin I2 receptor (IP, PRIPR)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

iloprost is developed for 3 unique indications across 3 therapeutic areas.

Therapeutic AreaConditionPhase
Injury, poisoning and procedural complicationsFrostbite✓ Approved
Vascular disordersRaynaud's phenomenonPhase III
Musculoskeletal and connective tissue disordersSclerodermaPhase III

Related Research Articles

PubMedEuropean journal of pharmacology2026-09-19

BASAL RELEASE OF 6-CYANODOPAMINE AND 6-NITRODOPAMINE FROM RAT ISOLATED AORTA AND THEIR ROLE IN VASCULAR RELAXATION.

Lima Antônio Tiago AT, Said George G, Britto-Júnior José J, Dos Santos Eric Xavier EX et al.

6-Cyanodopamine (6-CYD) and 6-nitrodopamine (6-ND) are newly described endogenous catecholamines. However, their presence and vascular actions in rat aorta remain unclear. Thoracic aortas from male Wistar rats were analyzed for basal catecholamine release by LC-MS/MS. Vascular reactivity was assessed in U-46619-precontracted rings with intact or removed endothelium and after pharmacological inhibition with Nω-nitro-L-arginine methyl ester (L-NAME), 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), indomethacin, SQ-22536, SCH-23390, and haloperidol. Tyrosine hydroxylase (TH) expression was examined by immunohistochemistry (IHC) and fluorescence in situ hybridization (FISH). Rat aorta basally released both 6-CYD and 6-ND, with 6-ND levels exceeding 6-CYD. Both catecholamines produced concentration-dependent relaxation, with 6-ND showing greater potency than 6-CYD (pEC50: 8.9±0.5 and 8.5±0.6, respectively). Endothelium removal abolished 6-CYD relaxation and significantly reduced 6-ND relaxation. L-NAME, ODQ, indomethacin, and SQ-22536 significantly inhibited responses to 6-CYD, but not to 6-ND, indicating different mechanisms of action. SQ-22536 also attenuated forskolin- and iloprost-induced relaxation, supporting involvement of adenylyl cyclase/cAMP signaling in 6-CYD responses. SCH-23390 had no effect on 6-CYD- and 6-ND-induced relaxation. Haloperidol reduced the effect of sumanirole- and 6-CYD-induced relaxation but had no effect on 6-ND-induced relaxation, suggesting involvement of D2-like receptor in 6-CYD signaling. Tyrosine hydroxylase protein and mRNA were detected by immunohistochemistry and fluorescent in situ hybridization respectively, in endothelial cells and adventitial neural structures. Rat thoracic aorta basally releases 6-CYD and 6-ND, and although both act as potent vasodilators, they have distinct mechanisms of action. These findings shed new light on mechanisms by which the vascular endothelium regulates vascular tone.

PMID 42762912
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PubMedDrug delivery and translational research2026-09-09

Aligning biopharma and academic partnerships to advance drug delivery technologies: insights from a multidisciplinary panel.

Steinbach-Rankins Jill M JM, Allen Christine J CJ, Prausnitz Mark R MR, Pettis Ronald J RJ et al.

The field of drug delivery is undergoing rapid transformation, driven by advances in biotherapeutics, new modalities, and innovative delivery technologies. However, translating these scientific breakthroughs into patient-centric therapies requires overcoming significant scientific, translational, and organizational barriers. This perspective piece provides insights from a multidisciplinary panel of leaders in biopharma, academia, and start-up innovation, focusing on the most promising opportunities and persistent challenges in the field. The discussion highlights the renewed and increased focus on subcutaneous and microneedle-based delivery systems, the evolving role of nanoparticle delivery, and the importance of aligning research with clinical and market needs through early cross-sector collaboration. The panel underscored the need for early stakeholder engagement, transparent communication, and iterative feedback to integrate business case considerations from the outset and foster successful partnerships. Various collaborative models that include pre-competitive consortia, open innovation incubators, public-private partnerships, and entrepreneurial training, are discussed for their effectiveness in bridging the gap between academic discovery and clinical translation. Ultimately, the advancement of drug delivery depends on multidisciplinary collaboration, robust translational frameworks, and sustained investment in innovative, patient-focused solutions that address real-world needs and improve patient outcomes.

PMID 42714736
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PubMedClinical and translational science2026-09-05

Expanding Quantitative Medicines' Reach: Systems and Methods to Enhance R&D Productivity and Decision-Making in the Agentic-Era.

Corrigan Brian W BW, Anderson Eric E, Tredennick Andrew A, Martinez Lomeli Luis L et al.

Despite integration of artificial intelligence (AI) into drug discovery and an expanding global medicines pipeline, new drug approvals have declined, highlighting a paradox in biopharma: More drugs discovered, but less approvals, higher costs, and longer timelines. Reasons for the decreased research and development (R&D) efficiency are multifactorial, in part driven by the complexity of new modalities, difficult targets and indications, and persistence of cognitive biases in clinical decision-making. One proposed solution to address R&D productivity challenges includes the adoption of organization-wide quantitative decision frameworks (QDFs). QDFs have the potential to increase R&D productivity by integrating quantitative assessments of program risk and value, clinical development costs, time, and probability of success into product valuations. A QDF integrates emerging clinical characteristics of the product through model-predicted efficacy and safety and links them to common valuation models to quantify the impact of product risk and uncertainty on value at different development stages. Context-aware AI can dynamically incorporate relevant unstructured information including clinical, competitor, market, and regulatory data into a QDF. The framework may be applied to compare clinical development scenarios for a single program, evaluate trade-offs between programs, and support portfolio-level decision making. Application of comprehensive QDFs in drug development promotes organizational alignment and transparency in product valuations, thereby supporting rationale decision-making, investment partnership negotiations, and product reimbursement assessment.

PMID 42698299
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PubMedCytokine2026-09-03

The clinical benefit of prostacyclin treatment in mechanically ventilated patients with SARS-CoV-2 infection is not attributed to anti-inflammatory effects.

Vigstedt Martin M, McGarrity Sarah S, Søe-Jensen Peter P, Bestle Morten H MH et al.

Treatment with the synthetic prostacyclin analog iloprost has been shown to attenuate endothelial glycocalyx shedding and organ failure in patients with critical Covid-19. The treatment is currently being investigated in a broader setting of patients with acute respiratory failure. We here investigated the effect on inflammatory and T-cell-derived cytokine and growth-factor responses in patients with critical Covid-19. Post-hoc analysis of a randomized controlled trial (n = 80) in mechanically ventilated patients with SARS-CoV-2 infection and concomitant endotheliopathy, defined as soluble thrombomodulin plasma-levels ≥4 ng/mL. Patients received 72 h iloprost infusion (1 ng/kg/min) or placebo. Blood samples were collected at baseline and 24 h after inclusion. Fifty-four cytokines and growth factors, distributed into six biomarker classes, were measured using the Meso Scale Discovery V-PLEX platform. Iloprost treatment, compared with placebo, did not result in statistically significant changes of any of the fifty-four measured biomarkers at 24 h, when adjusting for multiple testing. Likewise, linear mixed-effects models did not identify significant effects of iloprost on any of the six predefined biomarker classes at 24 h. In mechanically ventilated patients with SARS-CoV-2 infection and endotheliopathy, iloprost treatment had no detectable effect on inflammatory and T-cell-derived cytokine and growth-factor responses. The findings corroborate that the clinical benefit of iloprost is not attributed to anti-inflammatory effects. We suggest that future studies focus on patient selection for targeted treatment, and on combined treatment with anti-inflammatory and endothelium-stabilizing interventions, in patients with respiratory failure, hyperinflammation, and endotheliopathy.

PMID 42691796
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PubMedLancet (London, England)2026-08-28

Safety and lipoprotein(a)-lowering effects of Kylo-11, a non-canonical, long-duration small interfering RNA targeting lipoprotein(a): a first-in-human, randomised, double-blind, placebo-controlled, phase 1 trial.

Sarraju Ashish A, Du Xiaolin X, Zhou Luping L, Laffin Luke J LJ et al.

Elevated lipoprotein(a) concentrations are associated with the development of atherosclerotic cardiovascular disease. The aim of this study was to evaluate the safety and lipoprotein(a)-lowering effects of Kylo-11, a very long-acting small interfering RNA that targets lipoprotein(a). This randomised, double-blind, placebo-controlled, phase 1 trial was performed in a single hospital-based site in China in adults aged 18-55 years with elevated lipoprotein(a) concentrations who were otherwise healthy. Participants were randomly assigned to receive a single, subcutaneous dose of Kylo-11 or placebo (8:2) across seven dosing cohorts. Kylo-11 recipients could enter conditional extension follow-up up to day 337, whereas placebo recipients were followed up to day 169. Participants with lipoprotein(a) concentrations of 75-200 nmol/L were enrolled into cohorts 1-6 (ie, doses of 9, 30, 75, 225, 450, and 600 mg). Participants with lipoprotein(a) concentrations of more than 200 nmol/L were enrolled into cohort 7 (225 mg). The randomisation schedule was generated by an unmasked statistician with no involvement in study conduct, efficacy or safety analyses, or blinded data analysis, and assigned to treatment groups by an interactive web response system. Participants, investigators, and study personnel were masked to cohort assignment. The primary endpoint was the incidence of investigator-assessed adverse events within 24 weeks. All randomly assigned participants who received a dose of investigational product were included in the safety analysis set. All randomly assigned participants who received a dose of Kylo-11 and had at least one pharmacodynamic datapoint were included in the pharmacodynamic analysis set. Missing data were not imputed. The trial was registered on ClinicalTrials.gov (NCT06363851) and is now complete. Between May 30, 2024, and Dec 30, 2024, 71 participants were randomly assigned to the Kylo-11 cohorts (n=57) or the placebo cohort (n=14) and 70 participants received a dose. The median age of participants was 27·5 years (IQR 22·0-32·0), and 46 (65%) participants were male and 25 (35%) were female. Participants were followed up for a median of 337 days (IQR 334-337). 37 (53%) of 70 participants had adverse events up to 24 weeks, the majority of which were grade 1-2 and deemed unrelated to the study drug by the investigators. There were no injection-site reactions, no serious adverse events, no drug-related adverse events, and no deaths. Two grade 3 or higher events (ie, transient hypertriglyceridaemia at day 168 and elevated creatine phosphokinase at day 168) in the 225 mg cohort were adjudicated as unrelated to the study drug; one grade 3 or higher event (transient hypertriglyceridaemia) occurred in the placebo group at day 84. The prespecified pharmacodynamic secondary endpoints of median percent and absolute reductions in serum lipoprotein(a) over time at the final follow-up timepoint of 48 weeks for the Kylo-11 groups ranged from -53% (IQR -71 to -41) and -71 nmol/L (-79 to -60) in the 9 mg cohort to -97% (-98 to -97) and -129 nmol/L (-153 to -99) in the 600 mg cohort. In cohort 7 (225 mg; baseline lipoprotein(a) >200 nmol/L), the median reductions were -96% (-98 to -91) and -208 nmol/L (-222 to -198). A single dose of Kylo-11 was well tolerated, and at doses of 225 mg or higher, durably reduced serum lipoprotein(a) concentrations up to 48 weeks. Kylonova Biopharma.

PMID 42664979
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PubMedInternational journal of molecular sciences2026-08-27

Effects of Iloprost on TRPM7-Mediated Apoptosis and Oxidative Stress in an Experimental Testicular Torsion-Detorsion Model.

Kaya Tektemur Nalan N, Bilgetay Unlu Aysenur A, Kavak Balgetir Merve M, Tektemur Ahmet A et al.

Testicular torsion is a urological emergency that causes ischemia-reperfusion (I/R) injury and may result in irreversible germ cell loss and impaired fertility. Oxidative stress, inflammation, and apoptotic pathways play central roles in its pathogenesis. Transient Receptor Potential Melastatin-7 (TRPM7), a bifunctional ion channel/kinase, has recently been implicated in I/R-related cellular injury. Iloprost, a prostacyclin analogue with vasodilatory and antioxidant properties, may offer protective effects; however, its impact on TRPM7-mediated pathways in testicular I/R injury remains unclear. This study aimed to investigate the effects of iloprost on oxidative stress, apoptosis, and TRPM7 expression in an experimental testicular torsion-detorsion model. Thirty-five male Sprague Dawley rats were randomized into five groups: control, sham, iloprost, torsion-detorsion (T/D), and T/D + iloprost. After 60 min of torsion and subsequent detorsion, iloprost (2 µg/kg, intraperitoneal) was administered in the treatment group. Testicular tissues and serum samples were analyzed after 48 h. Histopathology (H&E), apoptosis (TUNEL assay), TRPM7 immunohistochemistry and mRNA expression (RT-qPCR), and serum total antioxidant status (TAS) and total oxidant status (TOS) were evaluated. Torsion-detorsion significantly increased TOS levels, apoptotic cell ratio (ACR), TRPM7 expression, and Bax mRNA expression, while reducing TAS levels (p < 0.05). Iloprost administration significantly improved oxidative stress parameters, restoring TAS and reducing TOS compared with the untreated T/D group. However, it did not significantly reduce histopathological damage, ACR, TRPM7 expression, or Bax mRNA expression. Bcl-2 expression remained largely unchanged across groups. Iloprost improved systemic oxidative status in testicular I/R injury but did not significantly attenuate TRPM7 expression, apoptotic changes, or structural damage under the experimental conditions used. The concurrent increase in TRPM7 expression and apoptotic indices following torsion-detorsion suggests an association between these alterations; however, the present study does not establish a causal relationship between TRPM7 and apoptosis. As TRPM7 activity was not directly assessed or experimentally manipulated, further studies involving TRPM7 inhibition or genetic silencing are required to determine its mechanistic role in testicular I/R-induced apoptosis.

PMID 42653455
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