ArticleImmunobiology2015
Compstatin analog Cp40 inhibits complement dysregulation in vitro in C3 glomerulopathy.
Article in Immunobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03316521 (Safety, Tolerability, Pharmacokinetics), which is not on this map. Cited by 34 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Safety, Tolerability, Pharmacokinetics (PK) and Pharmacodynamics (PD) of a Single Ascending Dose (SAD) and a Multiple Dose (MD) of the Complement Inhibitor AMY-101. A Prospective, Single-center, Open-label, First-In-Human (FIH) Clinical Study in Healthy Male Volunteers
Who cites it
34 citing papers in PubMed, 58 citations in OpenAlex.
- Differential effects of C5 inhibition, C3 inhibition, and alternative pathway inhibition on bacterial killing in vitro.Blood advances · 2025Article
- A novel complement C3 inhibitor CP40-KK protects against experimental pulmonary arterial hypertension via an inflammasome NLRP3 associated pathway.Journal of translational medicine · 2024Article
- Complement System Inhibitory Drugs in a Zebrafish (International journal of molecular sciences · 2023Article
- Therapeutic Potential of Targeting Complement C5a Receptors in Diabetic Kidney Disease.International journal of molecular sciences · 2023Review
- Protein therapeutics and their lessons: Expect the unexpected when inhibiting the multi-protein cascade of the complement system.Immunological reviews · 2023Review
- Exploiting protease activation for therapy.Drug discovery today · 2022Review
- Mechanisms Driving Neutrophil-Induced T-cell Immunoparalysis in Ovarian Cancer.Cancer immunology research · 2021Observational
- Aberrant Complement System Activation in Neurological Disorders.International journal of molecular sciences · 2021Review
- Computational analysis of complement inhibitor compstatin using molecular dynamics.Journal of molecular modeling · 2020Article
- A Narrative Review on C3 Glomerulopathy: A Rare Renal Disease.International journal of molecular sciences · 2020Review
- Heterogeneity in neutrophil responses to immune complexes.Blood advances · 2019Article
- Polyreactive IgM initiates complement activation by PF4/heparin complexes through the classical pathway.Blood · 2018Article
- Complement-mediated renal diseases after kidney transplantation - current diagnostic and therapeutic options inWorld journal of transplantation · 2018Review
- Thrombotic microangiopathy after renal transplantation: Current insights inWorld journal of transplantation · 2018Review
- Novel Immunoassay for Complement Activation by PF4/Heparin Complexes.Thrombosis and haemostasis · 2018Article
- Expanding Complement Therapeutics for the Treatment of Paroxysmal Nocturnal Hemoglobinuria.Seminars in hematology · 2018Review
- The renaissance of complement therapeutics.Nature reviews. Nephrology · 2018Review
- Kidney Diseases Associated With Alternative Complement Pathway Dysregulation and Potential Treatment Options.The American journal of the medical sciences · 2017Review
- Complement C3-Targeted Therapy: Replacing Long-Held Assertions with Evidence-Based Discovery.Trends in immunology · 2017Article
- Viral-derived complement inhibitors: current status and potential role in immunomodulation.Experimental biology and medicine (Maywood, N.J.) · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
C3 glomerulopathy (C3G) defines a group of untreatable ultra-rare renal diseases caused by uncontrolled activation of the alternative complement pathway. Nearly half of patients progress to end stage renal failure within 10 years. Cp40, a second-generation compstatin analog in clinical development, is a 14 amino-acid cyclic peptide that selectively inhibits complement activation in humans and non-human primates by binding to C3 and C3b. We hypothesized that by targeting C3 Cp40 would provide an effective treatment for C3G. By investigating its effects in vitro using multiple assays of complement activity, we show that Cp40 prevents complement-mediated lysis of sheep erythrocytes in sera from C3G patients, prevents complement dysregulation in the presence of patient-derived autoantibodies to the C3 and C5 convertases, and prevents complement dysregulation associated with disease-causing genetic mutations. In aggregate, these data suggest that Cp40 may offer a novel and promising therapeutic option to C3G patients as a disease-specific, targeted therapy. As such, Cp40 could represent a major advance in the treatment of this disease.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.