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

PubMedThe American journal of the medical sciences2026-10-02

Management of Pulmonary Hypertension in Interstitial Lung Disease Without Access to Inhaled Treprostinil: A Case Series from a Resource-Limited Setting.

Kabalak Pınar Akın PA, Söyler Yasemin Y, Cengiz Tuba İnal Tİ, Çelik Murat M et al.

Pulmonary hypertension (PH) may develop as a clinically important complication of parenchymal lung diseases, particularly in the setting of chronic hypoxemia and advanced interstitial lung disease. The management of interstitial lung disease-associated pulmonary hypertension (ILD-PH) remains challenging and requires a multidimensional assessment, including radiological findings, pulmonary function tests, comorbidities, and hemodynamic parameters. Although inhaled treprostinil is an approved treatment for ILD-PH, access to this therapy remains limited. We aimed to describe alternative management strategies and clinical outcomes in patients with ILD-PH in a resource-limited setting. This descriptive retrospective case series included four patients with different types of ILD: fibrotic hypersensitivity pneumonitis, combined pulmonary fibrosis and emphysema (CPFE), rheumatoid arthritis-associated ILD, and idiopathic pulmonary fibrosis (IPF). Demographic characteristics, hemodynamic data, treatment approaches, and clinical responses were evaluated. Inhaled iloprost was initiated in patients with IPF and fibrotic hypersensitivity pneumonitis. Both patients tolerated the treatment well and remained functionally stable. However, the patient with CPFE was unable to tolerate inhaled prostanoid therapy and had a fatal outcome despite treatment with a phosphodiesterase-5 inhibitor. The patient with rheumatoid arthritis-associated ILD had severe fibrotic parenchymal involvement and demonstrated clinical stability during a 6-month follow-up period under phosphodiesterase-5 inhibitor therapy. Patients with ILD-PH should be evaluated individually according to underlying lung pathology, disease phenotype, and treatment tolerability. Where inhaled treprostinil is unavailable, alternative therapies, such as inhaled iloprost or phosphodiesterase-5 inhibitors, may provide clinical benefits in selected patients. However, patients with CPFE may have poorer outcomes despite PH-targeted therapies.

PMID 42826861
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PubMedThe Lancet. Haematology2026-10-01

Felzartamab plus lenalidomide-dexamethasone versus lenalidomide-dexamethasone for relapsed or refractory multiple myeloma: an open-label, parallel-controlled, randomised, phase 3 trial.

He Haiyan H, Shang Jingjing J, Wang Yafei Y, Xia Zhongjun Z et al.

Complement-dependent cytotoxicity (CDC) of CD38 monoclonal antibodies has been associated with infusion-related reactions and might contribute to reduced clinical efficacy of CDC-reliant CD38 antibodies, particularly in patients with relapsed or refractory multiple myeloma with 1q21+. We aimed to evaluate felzartamab, a novel anti-CD38 monoclonal antibody that retains potent antibody-dependent cellular cytotoxicity and antibody-dependent cellular phagocytosis while exhibiting markedly attenuated CDC activity in Chinese patients with relapsed or refractory multiple myeloma. In this open-label, parallel-controlled, randomised, phase 3 trial conducted at 41 hospitals in China, adults aged 18 years or older with relapsed or refractory multiple myeloma who had received at least one previous line of systemic therapy, and were not refractory to lenalidomide were enrolled. Patients were randomly assigned (2:1) through a central interactive web response system, stratified by International Staging System stage, number of previous lines of therapy, and previous lenalidomide exposure, to receive intravenous felzartamab (16 mg/kg on days 1 and 4 during week 1, weekly week 2-12, every 2 weeks week 13-24, and every 4 weeks thereafter) plus once daily lenalidomide (25 mg orally on days 1-21 of each 28-day cycle) and once weekly oral dexamethasone (40 mg for patients aged ≤75 years and 20 mg for those >75 years) or lenalidomide and dexamethasone alone. The primary endpoint was progression-free survival, defined as the time from randomisation to disease progression or death from any cause, whichever occurred first, assessed by an independent review committee in the full analysis set (all randomly assigned patients who received at least one dose of study treatment). Safety was assessed in all patients who received at least one dose of study treatment. This trial is registered with ClinicalTrials.gov (NCT03952091) and is closed to enrolment. Between March 27, 2019, and Oct 20, 2021, 390 patients were assessed for eligibility, 295 of whom were enrolled and randomly assigned to felzartamab plus lenalidomide-dexamethasone (n=195) or lenalidomide-dexamethasone (n=100). The full analysis set included 289 patients (191 in the felzartamab plus lenalidomide-dexamethasone group and 98 in the lenalidomide-dexamethasone group). 185 (64%) of 289 patients were male, 104 (36%) were female, and all were of Asian ethnicity. At a median follow-up of 34·5 months (IQR 16·8-40·2) in the felzartamab plus lenalidomide-dexamethasone group and 28·7 months (10·8-38·8) in the lenalidomide-dexamethasone group, median progression-free survival was 18·9 months (95% CI 13·6-24·0) with felzartamab plus lenalidomide-dexamethasone versus 10·4 months (5·8-13·9) with lenalidomide-dexamethasone (hazard ratio 0·62 [95% CI 0·45-0·86]; p=0·0035). The most common grade 3-4 adverse events were neutropenia (105 [55%] of 192 vs 22 [23%] of 97), lymphopenia (79 [41%] vs 15 [15%]), leukopenia (74 [39%] vs 11 [11%]), thrombocytopenia (49 [26%] vs 11 [11%]), pneumonia (44 [23%] vs 13 [13%]), anaemia (33 [17%] vs 19 [20%]), hypokalaemia (30 [16%] vs ten [10%]), and upper respiratory tract infection (15 [8%] vs two [2%]). The most common serious adverse event was pneumonia (42 [22%] vs ten [10%]). Treatment-related deaths occurred in 11 (6%) of 192 patients in the felzartamab plus lenalidomide-dexamethasone group (five of unknown cause [possibly related to treatment], two due to pneumonia, one due to febrile infection, one due to cardiac arrest, one due to cerebral infarction, and one due to pneumonitis) and two (2%) of 97 patients in the lenalidomide-dexamethasone group (one due to pneumonia and one due to a fall]). Felzartamab plus lenalidomide-dexamethasone significantly prolonged progression-free survival compared with lenalidomide-dexamethasone alone, supporting felzartamab plus lenalidomide-dexamethasone as a potential new treatment option for Chinese patients with relapsed or refractory multiple myeloma. TJ Biopharma.

PMID 42822478
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PubMedBiotechnology and bioengineering2026-09-30

Mechanistic Digital Model for Real-Time Monitoring and Optimization of Adenovirus Production.

Xu Xingge X, Rüdiger Daniel D, Shin Jeongbin J, Chahal Shawninder S et al.

Adenoviral vectors are a critical vaccine platform, with billions of vaccine doses administered during the COVID-19 pandemic. In addition, they are promising therapeutics for cancer treatment. To advance their manufacturing, real-time monitoring of adenovirus production is essential for process optimization, yield improvement, and product quality assurance. However, despite modern bioreactors being equipped with advanced sensors, comprehensive monitoring of viral production in real-time remains limited. In this work, we investigated potential indicators of the cell density effect (CDE), which imposes a trade-off between high cell density and specific productivity, thereby hindering process optimization. Glucose availability (expressed as glucose per cell) at time of infection was identified as the most effective proxy indicator. We developed an age-structured mechanistic model linking measurable process variables, such as glucose and viable cell density to viral production while capturing the CDE. This framework enables the prediction of viral particle titers in both batch and fed-batch operation modes, achieving an RMSE of 0.39 in log10 IVP/mL for infectious viral particles and 0.20 in log10 VP/mL for total viral particles, corresponding to approximately 2.6 and 2.0 times the measurement standard deviation of the respective assays. The proposed model and calibration method lay the foundation for a digital twin of adenovirus production, bridging real-time sensing with model-based simulation to support adaptive control and accelerate the transition toward Biopharma 4.0.

PMID 42813361
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PubMedMedicines (Basel, Switzerland)2026-09-24

Pharmacotherapy of Kienböck Disease and the Carpal Avascular Necrosis Family: A Narrative Review with a Four-Axis Translation Framework.

Tenev Dimitar D, Hochbein Benedikt B, Enev Georgi G, Raykov Georgi G et al.

Background/Objectives: Kienböck disease (idiopathic avascular necrosis of the lunate) is treated almost exclusively surgically; its pharmacological evidence base comprises fewer than five primary publications and ~20 patient-level observations. Femoral-head, jaw, and knee osteonecrosis have decades of evidence, including randomised trials. We ask whether extra-carpal evidence can be translated to Kienböck disease and the wider Carpal Avascular Necrosis Family (lunate, scaphoid/Preiser, capitate, hamate, triquetrum). Methods: We conducted a narrative review reported per SANRA, searching PubMed, CrossRef, Google Scholar and three specialty registries from inception to 2026 across eleven drug classes and eleven skeletal sites. All references were independently verified against primary sources (PubMed/CrossRef). No Kienböck-specific randomised or controlled data exist; all conclusions therefore rest on indirect, extra-carpal evidence. Results: Three pathways (subchondral insufficiency fracture, microvascular ischaemia, hypercoagulability) predict drug-class plausibility differently by site. Iloprost is the candidate most consistently aligned across the translation axes, though no direct lunate data exist; teriparatide provides the only randomised evidence suggesting reversal of established osteonecrosis at any site (medication-related osteonecrosis of the jaw). The lunate sits within a coherent carpal AVN family sharing end-arterial supply, Lichtman-grade trajectories, and a near-identical evidence vacuum. Conclusions: A Four-Axis Translation Framework (mechanistic alignment, anatomic concordance, Lichtman-stage applicability, lunate-specific risk-benefit geometry) is proposed to evaluate which extra-carpal evidence is admissible at the lunate; with the carpal AVN family construct, these are the review's two novel contributions.

PMID 42783670
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PubMedESMO real world data and digital oncology2026-09-23

Clinical and genomic determinants of early treatment discontinuation in non-small-cell lung cancer: an analysis of the AACR Project GENIE Biopharma Collaborative NSCLC dataset.

Hamze D D, Mishra S S, Mohsin A A, Minuit S S et al.

Early treatment discontinuation (ETD) is common in cancer treatment but understudied. We sought to identify clinical and treatment-related factors associated with ETD in a real-world cohort of patients with non-small-cell lung cancer (NSCLC). We analyzed lines of therapy (LoTs) including drugs intended for an indefinite treatment sourced from the American Association for Cancer Research Project Genomics Evidence Neoplasia Information Exchange Biopharma Collaborative NSCLC cohort. Associations between treatment exposure and ETD were evaluated using multivariable logistic regression adjusting for age at LoT initiation, sex, stage, and context (first-line, second-line, third-line, or later). Sensitivity analyses examined mutation-specific targeted therapy exposures and ETD within 14 days of death. ETD occurred in 883 of 2098 eligible LoTs (42%). Programmed cell death protein 1/programmed death-ligand 1 inhibitor exposure was associated with higher odds of ETD [odds ratio (OR) = 2.07, 95% confidence interval (CI) 1.27-3.38], whereas small-molecule inhibitor exposure was associated with lower odds (OR = 0.43, 95% CI 0.26-0.70). Context showed a graded increase in ETD risk: second-line versus first-line (OR = 1.46, 95% CI 1.14-1.87) and third-line or later versus first-line (OR = 2.63, 95% CI 2.09-3.32). In 302 LoTs with an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) in patients with EGFR-activating mutations, EGFR TKI naivety was associated with lower odds of ETD (OR = 0.34, 95% CI 0.19-0.59). Eighty LoTs ended within 14 days of death, of which 54 (68%) were ETDs. ETD in NSCLC is associated with treatment modality, timing, and biology. The drivers of ETD are complex and span medical, social, and psychological domains. This study highlights ETD as a measurable quantity and provides a framework for future studies.

PMID 42774563
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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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