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Modified compstatin with peptide backbone and C-terminal modifications - Lambris John D., Qu Hongchang

Modified compstatin with peptide backbone and C-terminal modifications - Lambris John D., Qu Hongchang | Complement | Scoop.it

Compounds comprising peptides capable of binding C3 protein and inhibiting complement activation are disclosed. These compounds display greatly improved complement activation-inhibitory activity as compared with currently available compounds. The compounds comprise compstatin analogs having a constrained backbone at position 8 (glycine) and, optionally, specific substitutions for threonine at position 13.

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Therapeutic C3 inhibitor Cp40 abrogates complement activation induc... - PubMed - NCBI

Immunobiology. 2014 Nov 3. pii: S0171-2985(14)00224-1. doi: 10.1016/j.imbio.2014.10.026. [Epub ahead of print]
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Complete complement inhibition in response to hemodialysis filters by Cp40 (AMY-101)

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Therapeutic C3 inhibitor Cp40 abrogates complement activation induced by modern hemodialysis filters

Therapeutic C3 inhibitor Cp40 abrogates complement activation induced by modern hemodialysis filters | Complement | Scoop.it

Abstract

Approximately 350,000 individuals in the United States rely on maintenance hemodialysis treatment because of end-stage renal disease. Despite improvements in dialysis technology, the mortality rate for patients treated with maintenance dialysis is still exceptionally high, with a 5-year survival rate of only 35%. Many patients succumb to conditions resulting at least in part from the chronic induction of inflammation. Among the triggers of inflammation, the complement system is of particular importance, being a well-appreciated mediator of inflammatory processes that is involved in many pathologic states. Here we used a refined pre-clinical model of hemodialysis in cynomolgus monkeys to confirm that even modern, polymer-based hemodialysis filters activate complement and to evaluate the potential of Cp40, a peptidic C3 inhibitor, to attenuate hemodialysis-induced complement activation. Our data show marked induction of complement activation even after only a single session of hemodialysis. Importantly, complete inhibition of complement activation was achieved in response to two distinct Cp40 treatment regimens. Further, we show that application of Cp40 during hemodialysis resulted in increased levels of the anti-inflammatory cytokine IL-10, indicating that Cp40 may be a potent and cost-effective treatment option for attenuating chronic inflammatory conditions in dialysis-dependent patients.

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FDA grants orphan drug designation for PNH to Amyndas Pharmaceuticals’ novel complement inhibitor

FDA grants orphan drug designation for PNH to Amyndas Pharmaceuticals’ novel complement inhibitor | Complement | Scoop.it

Amyndas Pharmaceuticals SA, the complement therapeutics company, announced that the U.S. Food and Drug Administration (FDA) has granted AMY-101, a potent complement C3 inhibitor, an Orphan Drug Designation for the treatment of Paroxysmal Nocturnal Hemoglobinuria (PNH). The U.S. FDA orphan designation comes after the European Medicines Agency (EMA) orphan status approval of AMY-101 for the same indication, less than 2 months ago.

“We are pleased to receive orphan drug designation for AMY-101 and are encouraged by the FDA’s recognition for the need of innovative new treatments for PNH” said Dr. Lambris, Founder of Amyndas and Professor of Research Medicine in the Department of Pathology and Laboratory Medicine at the University of Pennsylvania. In PNH, it is clear that about 30 percent of the patients are not optimally responding to therapy; when current treatment fails, clinicians have limited options to offer these patients. AMY-101 acts through a novel mechanism of action, inhibiting complement centrally, at the level of C3 instead of C5; this approach could increase the number of PNH therapy responders and benefit many more patients suffering from PNH”.

for more click here http://www.fiercepharma.com/press-releases/fda-grants-orphan-drug-designation-pnh-amyndas-pharmaceuticals-novel-comple

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Hematology Times - New approach for treating PNH

Hematology Times - New approach for treating PNH | Complement | Scoop.it

Investigators have identified a novel strategy for treating paroxysmal nocturnal hemoglobinuria (PNH), according to a paper published inBlood

In patients with PNH, defective expression of regulatory proteins on the surface of red blood cells leaves the cells vulnerable to attack by the complement immune system. 

This can lead to hemolysis, which results in severe anemia and contributes to a high risk of thrombosis. 

Eculizumab is the only approved therapeutic for PNH. The drug reduces hemolysis and can provide patients with relief from blood transfusions. 

However, eculizumab is costly (currently more than $400,000 per year per patient), and one third of PNH patients who receive eculizumab continue to require blood transfusions to manage their anemia. 

Investigators previously discovered that this non-response is due to fragments of complement C3 proteins on the surface of red blood cells, which are eventually attacked by immune cells.

Therefore, John Lambris, PhD, of the University of Pennsylvania, and his colleagues hypothesized that using small molecules to inhibit the complement cascade at the level of C3 proteins might be an effective strategy for treating PNH.  

The team thought this method would prevent both hemolysis and immune cell recognition, and it might be more cost-effective than the current antibody-based treatment.

So they investigated the effect of a C3 inhibitor called Cp40 and its long-acting form, PEG-Cp40, on self-attack and resulting hemolysis using human PNH cells. Both compounds effectively inhibited hemolysis and efficiently prevented deposition of C3 fragments on PNH red blood cells. 

In non-human primates, a single injection of PEG-Cp40 had an elimination half-life of more than 5 days. However, the investigators found evidence to suggest the drug may affect plasma levels of C3. 

“We think these 2 compounds are excellent and potentially cost-effective candidates for further clinical investigation,” Dr Lambris said. 

He hopes the compounds will be tested in clinical trials by 2015. Dr Lambris and his colleague, Daniel Ricklin, PhD, are the inventors of patents and patent applications owned by the University of Pennsylvania that describe the use of complement inhibitors for therapeutic purposes. 

And Dr Lambris is a founder and equity holder of Amyndas Pharmaceuticals, which has exclusively licensed the Cp40 and PEG-Cp40 technologies from the university and is developing complement inhibitors for clinical applications.

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Complement in paroxysmal nocturnal hemoglobinuria: exploiting our current knowledge to improve the treatment landscape, Expert Review of Hematology, Informa Healthcare

Complement in paroxysmal nocturnal hemoglobinuria: exploiting our current knowledge to improve the treatment landscape, Expert Review of Hematology, Informa Healthcare | Complement | Scoop.it
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October 2014, Vol. 7, No. 5 , Pages 583-598 (doi:10.1586/17474086.2014.953926)
Dimitrios C Mastellos1Daniel Ricklin2Despina Yancopoulou3Antonio Risitano4 and John D Lambris *2
Paroxysmal nocturnal hemoglobinuria (PNH) is a rare hematological disorder associated with an acquired deficiency in glycophosphatidylinositol-anchor biosynthesis that renders erythrocytes susceptible to complement attack. Intravascular hemolysis via the membrane attack complex is a clinical hallmark of the disease, and C5 blockade is currently the only approved treatment for PNH. However, residual anemia is an emerging observation for many PNH patients receiving anti-C5 treatment. A range of complement-targeted therapeutic approaches, encompassing surface-directed inhibition of C3 convertases, blockade of membrane attack complex assembly or C3 interception using peptidic inhibitors, has yielded promising results and offers leverage for even more effective treatment of PNH. This article discusses recent advances in this rapidly evolving field, integrating critical perspectives from preclinical PNH models and diverse complement modulation strategies with genetic insights and therapy response profiles. It also evaluates the relative efficacy, limitations and benefits afforded by C3 or C5 inhibition in the context of PNH therapeutics.




Read More: http://informahealthcare.com/doi/abs/10.1586/17474086.2014.953926

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Drug for Rare Blood Disorder Developed at Penn Receives Orphan Drug Status from European Union

A Penn Medicine-developed drug has received orphan status in Europe this week for the treatment of paroxysmal nocturnal hemoglobinuria (PNH), a rare, life-threatening disease that causes anemia due to destruction of red blood cells and thrombosis.
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Porphyromonas gingivalis manipulates compl... [Cell Host Microbe. 2014] - PubMed - NCBI

Certain low-abundance bacterial species, such as the periodontitis-associated oral bacterium Porphyromonas gingivalis, can subvert host immunity to remodel a normally symbiotic microbiota into a dysbiotic, disease-provoking state. However, such pathogens also exploit inflammation to thrive in dysbiotic conditions. How these bacteria evade immunity while maintaining inflammation is unclear. As previously reported, P. gingivalis remodels the oral microbiota into a dysbiotic state by exploiting complement. Now we show that in neutrophils P. gingivalis disarms a host-protective TLR2-MyD88 pathway via proteasomal degradation of MyD88, whereas it activates an alternate TLR2-Mal-PI3K pathway. This alternate TLR2-Mal-PI3K pathway blocks phagocytosis, provides "bystander" protection to otherwise susceptible bacteria, and promotes dysbiotic inflammation in vivo. This mechanism to disengage bacterial clearance from inflammation required an intimate crosstalk between TLR2 and the complement receptor C5aR and can contribute to the persistence of microbial communities that drive dysbiotic diseases.

Copyright © 2014 Elsevier Inc. All rights reserved.

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Porphyromonas gingivalis manipulates compl... [Cell Host Microbe. 2014] - PubMed - NCBI

Porphyromonas gingivalis manipulates compl... [Cell Host Microbe. 2014] - PubMed - NCBI | Complement | Scoop.it
PubMed comprises more than 23 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
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Amyndas developing super compstatins for complement-mediated disorders - BioCentury.com

Amyndas developing super compstatins for complement-mediated disorders - BioCentury.com | Complement | Scoop.it

Transatlantic sister companies Amyndas Pharmaceuticals S.A. and Amyndas Pharmaceuticals LLC are developing therapies to treat complement-mediated disorders that could be more potent than other complement inhibitors, potentially opening up new indications.

Lead candidate Amanden comes from a class of synthetic analogs of the peptidiccomplement 3 (C3) inhibitor compstatin, which the company calls super compstatins.

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Aegean Conferences: 8th International Conference on Complement Therapeutics

Aegean Conferences: 8th International Conference on Complement Therapeutics | Complement | Scoop.it

The 8th Annual International Innate Immunity Conference will be held at the Avra Hotel in Chania, Greece , from  September 1-6, 2015. The Conference is under the sponsorship of Aegean Conferences (www.aegeanconferences.org), a non-profit educational organization promoting science through focused scientific conferences (please visit www.aegeanconferences.org and click on News, on the top right hand corner, for meeting reports  of previous Aegean Conferences.


The past decade has witnessed a new surge in the development of complement-targeted therapeutics, fueled by the successful launch of first complement drugs and the discovery of both orphan and highly prevalent diseases with contribution of complement. Apart from offering new hope for patients suffering from such diseases, the study of complement pathways, mutations, and deficiencies also teaches us important lessons about the role of complement in health and disease and allows us to refine our models and tools for applied and basic research. This conference aims to bring together academic and industry scientists and clinical development experts who are focused on contemporary and emerging aspects of complement-mediated disease pathogenesis and the development of therapeutics that modulate this system in a beneficial manner. Topics discussed during the conference include: targets, mechanisms & delivery options; therapeutic approaches & pipeline compounds; infections, periodontal diseases & sepsis; autoimmune & blood disorders (e.g. lupus, PNH); inflammatory diseases (e.g. asthma, arthritis); ocular diseases (e.g. AMD); kidney diseases (e.g. aHUS, MPGN II); neurological diseases (e.g. Alzheimer’s); metabolic & cardiovascular diseases; organ/cell transplantation & I/R injury; biomaterials & drug delivery devices;  diagnostics & imaging.


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Perelman School wins $10M renewal to study oldest part of human immune ... - News-Medical.net

Perelman School wins $10M renewal to study oldest part of human immune ... - News-Medical.net | Complement | Scoop.it
Perelman School wins $10M renewal to study oldest part of human immune ...
News-Medical.net
John Lambris, PhD, the Dr.

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Conjugation to Albumin-Binding Molecule Tags as a Strategy to Improve Both Efficacy and Pharmacokinetic Properties of the Complement Inhibitor Compstatin - Huang - 2014 - ChemMedChem - Wiley Online...

Conjugation to Albumin-Binding Molecule Tags as a Strategy to Improve Both Efficacy and Pharmacokinetic Properties of the Complement Inhibitor Compstatin - Huang - 2014 - ChemMedChem - Wiley Online... | Complement | Scoop.it

The compstatin family of complement inhibitors has shown promise in various immuno-inflammatory disorders. Although recent analogues show beneficial pharmacokinetics, further extension of the plasma half-life is expected to benefit systemic application of these peptidic inhibitors. We therefore synthesized conjugates of compstatin analogues and albumin-binding molecules (ABM) to increase circulatory residence. Equilibrium dialysis in complement-depleted serum showed a marked increase in plasma protein binding from <8 % to >99 % for a resulting chimera (ABM2-Cp20). Further analysis confirmed interaction with albumin from different species, primarily via site II. Importantly, ABM2-Cp20 bound 20-fold stronger to its target protein C3b (KD =150 pM) than the parent peptide. Kinetic and in silico analysis suggested that ABM2 occupies a secondary site on C3b and improves the dissociation rate via additional contacts. Addition of an ABM modifier thereby not only improved plasma protein binding but also produced the most potent compstatin analogue to date with potential implications for the treatment of systemic complement-related diseases.

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New book on 'Innate Immunity and Inflammation' from Cold Spring Harbor ... - Phys.Org

New book on 'Innate Immunity and Inflammation' from Cold Spring Harbor ... - Phys.Org | Complement | Scoop.it
Phys.org Science News Wire : New book on 'Innate Immunity and Inflammation' from Cold Spring Harbor Laboratory Press -- a press release is provided to you ìas isî with little or no review from Phys.org staff.

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Gilbert C FAURE's curator insight, December 4, 2014 3:35 PM

Written and edited by experts in the field, Innate Immunity and Inflammation, published by Cold Spring Harbor Laboratory Press, reviews the cellular and molecular mechanisms involved in innate immunity and all types of inflammation. The contributors examine the cell types that make up the innate immune system, their use of pattern recognition receptors (e.g., Toll-like receptors) to identify pathogens and damaged tissues, and how they trigger signaling pathways that culminate in inflammation, pathogen destruction, and tissue repair. The numerous chemical signals and factors involved in innate immunity and inflammation are described, as are those that keep inflammation in check.

The authors also discuss the diseases that can result when these processes go awry, such as rheumatoid arthritis and cancer. This volume is therefore a valuable reference for all immunologists, cell biologists, and medical scientists wishing to understand these protective processes and their implications for human health and disease.

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Dramatic effects of eculizumab in a child with diffuse proliferativ... - PubMed - NCBI

Pediatr Nephrol. 2015 Jan;30(1):167-72. doi: 10.1007/s00467-014-2944-y. Epub 2014 Aug 31.
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Abstract
BACKGROUND: 

Treatment of systemic lupus erythematosus (SLE) with severe diffuse proliferative nephritis is often challenging, particularly in small children in whom a genetic conditioning is likely to play a role. The effectiveness of standard therapy based on glucocorticoid and immunosuppressive drugs is often unsatisfactory.

CASE: 

A 4 year-old girl, whose parents were first-grade cousins of Moroccan ancestry, developed SLE that progressed to severe renal involvement despite standard therapy. She had persistently undetectable serum C4 levels and very low C3 levels (<30 mg/dl), and extremely high anti-DNA titers (>1:640) that remained unmodified during 2 years of follow-up. No mutations of genes encoding for complement inhibitors were detected. Despite aggressive therapy based on prednisone, plasma exchanges, and cyclosporine, the child worsened and eventually developed features of atypical hemolytic uremic syndrome (aHUS). Treatment with eculizumab provided prompt remission of vasculitis, proteinuria, and hematuria, with normalization of renal function. Two attempts to withdraw eculizumab were followed by severe relapses and rescued by reinstating treatment. The child has been treated with eculizumab for > 17 months without relevant side effects.

CONCLUSION: 

C5 inhibition by eculizumab completely reversed clinical symptoms and laboratory renal signs of severe lupus nephritis. Blocking complement-system activation with the use of targeted drugs may be a new and exciting strategy to treat SLE patients unresponsive to conventional therapy.


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Complement in paroxysmal nocturnal hemogl... [Expert Rev Hematol. 2014] - PubMed - NCBI

Abstract

Paroxysmal nocturnal hemoglobinuria (PNH) is a rare hematological disorder associated with an acquired deficiency in glycophosphatidylinositol-anchor biosynthesis that renders erythrocytes susceptible to complement attack. Intravascular hemolysis via the membrane attack complex is a clinical hallmark of the disease, and C5 blockade is currently the only approved treatment for PNH. However, residual anemia is an emerging observation for many PNH patients receiving anti-C5 treatment. A range of complement-targeted therapeutic approaches, encompassing surface-directed inhibition of C3 convertases, blockade of membrane attack complex assembly or C3 interception using peptidic inhibitors, has yielded promising results and offers leverage for even more effective treatment of PNH. This article discusses recent advances in this rapidly evolving field, integrating critical perspectives from preclinical PNH models and diverse complement modulation strategies with genetic insights and therapy response profiles. It also evaluates the relative efficacy, limitations and benefits afforded by C3 or C5 inhibition in the context of PNH therapeutics.

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Drug for rare blood disorder gets EU orphan status 

Drug for rare blood disorder gets EU orphan status  | Complement | Scoop.it
A DRUG for rare blood disorder developed at Penn Medicine has this week received orphan drug status in the European Union. The compound, called AMY-101, is...
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Gilbert C FAURE's comment, September 22, 2014 5:06 AM
congrats
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Crosstalk between the coagulation and complement systems in sepsis - Thrombosis Research


Sepsis is a potent activator of the hemostatic and complement systems. While local activation of these proteolytic cascades contributes to the host defense, their uncontrolled systemic activation has major tissue damaging effects that lead to multiple organ failure and death. We have extensively studied the activation of complement and coagulation cascades in experimental sepsis using baboons challenged with live bacteria, such as Gram-negative Escherichia coli or Gram-positive Staphylococcus aureus and Bacillus anthracis, or with the bacterial product peptidoglycan. We observed that these challenges rapidly induce disseminated intravascular coagulation and robust complement activation. We applied a potent C3 convertase inhibitor, compstatin, which prevented sepsis-induced complement activation, reduced thrombocytopenia, decreased the coagulopathic responses, and preserving the endothelial anticoagulant properties. Overall, our work demonstrates that live bacteria and bacterial products activate the complement and coagulation cascades, and that blocking formation of complement activation products, especially during the organ failure stage of severe sepsis could be a potentially important therapeutic strategy.

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Complement Patent Datbase

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Gilbert C FAURE's curator insight, August 29, 2014 4:07 AM

thanks for sharing this curated database of patents specifically dedicated to complement

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EMA grants orphan drug designation for PNH to Amyndas Pharmaceuticals’ novel complement inhibitor | PRLog

EMA grants orphan drug designation for PNH to Amyndas Pharmaceuticals’ novel complement inhibitor. Amyndas Pharmaceuticals SA, the complement therapeutics company, announced that the European Medicines Agency (EMA) has granted AMY-101, a potent complement C3 inhibitor, an Orphan Drug Designation for the treatment of Paroxysmal Nocturnal Hemoglobinuria. - PR12364497
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Genetic and intervention studies implicating compl... [J Immunol. 2014] - PubMed - NCBI

Genetic and intervention studies implicating compl... [J Immunol. 2014] - PubMed - NCBI | Complement | Scoop.it

Chronic periodontitis is induced by a dysbiotic microbiota and leads to inflammatory destruction of tooth-supporting connective tissue and bone. The third component of complement, C3, is a point of convergence of distinct complement activation mechanisms, but its involvement in periodontitis was not previously addressed. We investigated this question using two animal species models, namely, C3-deficient or wild-type mice and nonhuman primates (NHPs) locally treated with a potent C3 inhibitor (the compstatin analog Cp40) or an inactive peptide control. In mice, C3 was required for maximal periodontal inflammation and bone loss, and for the sustenance of the dysbiotic microbiota. The effect of C3 on the microbiota was therefore different from that reported for the C5a receptor, which is required for the initial induction of dysbiosis. C3-dependent bone loss was demonstrated in distinct models, including Porphyromonas gingivalis-induced periodontitis, ligature-induced periodontitis, and aging-associated periodontitis. Importantly, local treatment of NHPs with Cp40 inhibited ligature-induced periodontal inflammation and bone loss, which correlated with lower gingival crevicular fluid levels of proinflammatory mediators (e.g., IL-17 and RANKL) and decreased osteoclastogenesis in bone biopsy specimens, as compared with control treatment. To our knowledge, this is the first time, for any disease, that complement inhibition in NHPs was shown to inhibit inflammatory processes that lead to osteoclastogenesis and bone loss. These data strongly support the feasibility of C3-targeted intervention for the treatment of human periodontitis.

Copyright © 2014 by The American Association of Immunologists, Inc.

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Peptide inhibitors of C3 activation as a novel strategy of complement ...

Peptide inhibitors of C3 activation as a novel strategy of complement ... | Complement | Scoop.it
Paroxysmal nocturnal hemoglobinuria (PNH) is characterized by complement-mediated intravascular hemolysis due to the lack of CD55 and CD59 on affected erythrocytes. The anti-C5 antibody eculizumab has proven ...

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Gilbert C FAURE's curator insight, November 11, 2014 2:37 AM
Abstract

Paroxysmal nocturnal hemoglobinuria (PNH) is characterized by complement-mediated intravascular hemolysis due to the lack of CD55 and CD59 on affected erythrocytes. The anti-C5 antibody eculizumab has proven clinically effective, but uncontrolled C3 activation due to CD55 absence may result in opsonization of erythrocytes, possibly leading to clinically meaningful extravascular hemolysis. We investigated the effect of the peptidic C3 inhibitor, compstatin Cp40, and its long-acting form (polyethylene glycol [PEG]-Cp40) on hemolysis and opsonization of PNH erythrocytes in an established in vitro system. Both compounds demonstrated dose-dependent inhibition of hemolysis with IC50 ∼4 µM and full inhibition at 6 µM. Protective levels of either Cp40 or PEG-Cp40 also efficiently prevented deposition of C3 fragments on PNH erythrocytes. We further explored the potential of both inhibitors for systemic administration and performed pharmacokinetic evaluation in nonhuman primates. A single intravenous injection of PEG-Cp40 resulted in a prolonged elimination half-life of >5 days but may potentially affect the plasma levels of C3. Despite faster elimination kinetics, saturating inhibitor concentration could be reached with unmodified Cp40 through repetitive subcutaneous administration. In conclusion, peptide inhibitors of C3 activation effectively prevent hemolysis and C3 opsonization of PNH erythrocytes, and are excellent, and potentially cost-effective, candidates for further clinical investigation.

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Two-pronged Amyndas targets complement-based anti-inflammatories

Two-pronged Amyndas targets complement-based anti-inflammatories | Complement | Scoop.it

Researcher John Lambris has devoted his career of more than 30 years to exploring the human complement system. His lab at the University of Pennsylvania, where Lambris serves as professor of research medicine in the department of pathology and laboratory medicine, was among the first in the world to map the critical sites on the human C3 protein that are responsible for its many functions and to define its complex binding dynamics to various C3 natural ligands.

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Aegean Conferences: 12th Innate Immunity Conference

Aegean Conferences: 12th Innate Immunity Conference | Complement | Scoop.it

Tthe 12th Annual International Innate Immunity Conference will be held at the Avra Hotel in Chania, Greece , from June 19-24, 2015. The Conference is under the sponsorship of Aegean Conferences (www.aegeanconferences.org), a non-profit educational organization promoting science through focused scientific conferences (please visit www.aegeanconferences.org and click on News, on the top right hand corner, for meeting reports  of previous Aegean Conferences.

The topics to be covered during the next meeting are:

·  Evolution of innate immune systems

·  Structural biology

·  Host-microbe interactions

·  Pattern-recognition receptors

·  Crosstalk pathways in innate immunity

·  Interactions with adaptive immunity

·  Inflammation and pathophysiology

·  Therapeutic applications


The purpose of the 12th Innate Immunity is to bring together scientists from all over the world to discuss their latest findings on the various aspects of Innate Immunity. The specific topics include:  Evolution of the innate immune system,  Host-microbe interactions, Interactions with adaptive immunity, Pathophysiology-Inflammation, Structural biology, and Therapeutic applications. Abstracts are invited from the international community for all these topics. The scientific sessions will convene in the mornings and early afternoons and will include lectures by invited speakers, as well as talks and poster presentations selected from submitted abstracts. The conference has limited participation and a scientific and social program that will maximize scientific interchange. In order to encourage the participation of young scientists, the Aegean Conferences is offering Trainee Travel Awards to offset a portion of the travel expenses to the Conference. The Conference Organizing Committee will select the Award recipients based on the scientific merit of abstracts submitted by applicants.

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$10 Million Renewal for Penn Medicine Program Studying Immune System - UPENN Almanac

$10 Million Renewal for Penn Medicine Program Studying Immune System - UPENN Almanac | Complement | Scoop.it
$10 Million Renewal for Penn Medicine Program Studying Immune System UPENN Almanac John Lambris, the Ralph and Sallie Weaver Professor of Research Medicine in the department of pathology and laboratory medicine, has been studying the complement...

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Gilbert C FAURE's curator insight, July 16, 2014 12:46 PM

money to study complement!!