DOCSLIB.ORG

Targeting Degraded Collagen with Collagen Hybridizing Peptides (CHP)

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Targeting Degraded Collagen with Collagen Hybridizing Peptides (CHP) 1 2 Product flyer 3 4 5 6 7 Targeting degraded collagen with 8 Collagen Hybridizing Peptides (CHP) 9 10 11 12 13 14 15 16 17 18 19 20 21 Special features Applications 22 A non-antibody approach without Histopathology: CHP marks tissue damage species restrictions and remodeling during pathological and physiological events[1,2] 23 Relies on collagen’s secondary triple helix structure instead of a defined Collagen identification: CHP visualizes 24 sequence collagen bands of all types in SDS-PAGE with high specificity[3] High affinity with essentially no 25 nonspecific binding Mechanical damage: CHP enables measuring and localizing of mechanical 26 Applicable to nearly every tissue type injury to collagenous tissue at molecular Suitable for both frozen and paraffin- level in various tissues (e.g. bone, cartilage, 27 embedded sections tendon, ligament, blood vessel, skin etc.)[4] 28 Stable at 4 °C, no need to aliquot for Tissue decellularization: CHP allows storage direct and quantitative assessment of denatured collagen in ECM materials[5] 29 30 31 version 1; page 1 of 2 32 33 34 Product flyer 35 36 37 Targeting degraded collagen with Collagen Hybridizing Peptide (CHP) 38 Collagen is the most abundant protein in mammals. It is the major structural component of almost all organs and tissues. Excessive collagen degradation is implicated in a variety of pathological 39 conditions, such as cancer, arthritis and fibrosis[6]. 40 The triple helix is the hallmark structure of collagen. During tissue remodeling, the triple helical 41 collagen molecules are degraded by specific proteases (e.g. MMP or cathepsin K) and become unfolded at body temperature. The Collagen Hybridizing Peptide (CHP) is a synthetic peptide 42 that can specifically bind to such denatured collagen strands through hydrogen bonding in histology[1], in vivo[2], and in vitro (3D cell culture)[7]. CHP is an extremely specific probe for 43 unfolded collagen: it has negligible affinity to intact collagen molecules due to the lack of binding sites; it is also inert towards non-specific binding because of its neutral and hydrophilic nature[3]. 44 Principle of the Collagen Hybridizing Peptide (CHP) 45 By sharing the structural and sequence motif of natural 46 collagen, CHP has a strong capability to hybridize with denatured collagen strands, in a fashion that is similar to 47 a DNA fragment annealing to its complimentary DNA strand during PCR. 48 49 CHP is a powerful histopathology tool which enables straightforward detection of tissue 50 damage caused by a large variety of diseases, as well as tissue remodeling during development and aging[2]. 51 In cell imaging, CHP robustly visualizes the pericellular collagen turnover caused by proteolytic 52 migration of cancer cells within 3D collagen matrix, without the use of synthetic fluorogenic matrices or genetically modified cells[7]. 53 References 54 1. In situ imaging of tissue remodeling with collagen hybridizing peptides. ACS Nano, 2017. 2. Targeting collagen strands by photo-triggered triple-helix hybridization. Proc. Natl. Acad. Sci. U.S.A., 2012. 3. Direct detection of collagenous proteins by fluorescently labeled collagen mimetic peptides. Bioconjug. Chem., 2013. 55 4. Molecular level detection and localization of mechanical damage in collagen enabled by collagen hybridizing peptides. Nat. Commun., 2017. 56 5. Molecular assessment of collagen denaturation in decellularized tissues using a collagen hybridizing peptide. Acta Biomater., 2017. 6. Targeting and mimicking collagens via triple helical peptide assemblies. Curr. Opin. Chem. Biol., 2013. 57 7. Visualizing collagen proteolysis by peptide hybridization: From 3D cell culture to in vivo imaging. Biomaterials, 2018. 58 Available products 59 Item Description Regulatory status Package size Product Code Collagen Hybridizing Peptide, CHP coupled with 5 FAM 60 μg FLU60 5 FAM Conjugate (F-CHP)1 for immunofluorescence [RUO] 60 300 μg FLU300 Collagen Hybridizing Peptide, CHP coupled with Cy3 for 60 μg RED60 61 Cy3 Conjugate (R-CHP)1 immunofluorescence [RUO] 300 μg RED300 Collagen Hybridizing Peptide, CHP coupled with biotin for 62 60 μg BIO60 Biotin Conjugate (B-CHP)1 immunohistochemistry and [RUO] SDS-PAGE 300 μg BIO300 63 1 Distributed for 3Helix Inc., Salt Lake City, USA version 1; page 2 of 2 .
Load more

Recommended publications
  • Collagen and Elastin Fibres
    J Clin Pathol: first published as 10.1136/jcp.s3-12.1.49 on 1 January 1978. Downloaded from J. clin. Path., 31, Suppl. (Roy. Coll. Path.), 12, 49-58 Collagen and elastin fibres A. J. BAILEY From the Agricultural Research Council, Meat Research Institute, Langford, Bristol Although an understanding of the intracellular native collagen was generated from type I pro- biosynthesis of both collagen and elastin is of collagen. Whether this means that the two pro- considerable importance it is the subsequent extra- collagens are converted by different enzyme systems cellular changes involving fibrogenesis and cross- and the type III enzyme was deficient in these linking that ensure that these proteins ultimately fibroblast cultures, or that the processing of pro become the major supporting tissues of the body. type III is extremely slow, is not known. The latter This paper summarises the formation and stability proposal is consistent with the higher proportion of collagen and elastin fibres. of soluble pro type III extractable from tissue (Lenaers and Lapiere, 1975; Timpl et al., 1975). Collagen Basement membrane collagens, on the other hand, do not form fibres and this property may be The non-helical regions at the ends of the triple due to the retention of the non-helical extension helix of procollagen probably provide a number of peptides (Kefalides, 1973). In-vivo biosynthetic different intracellular functions-that is, initiating studies showing the absence of any extension peptide rapid formation of the triple helix; inhibiting intra- removal support this (Minor et al., 1976), but other cellular fibrillogenesis; and facilitating transmem- workers have reported that there is some cleavage brane movement.
    [Show full text]
  • Evaluation of Elastin/Collagen Content in Human Dermis In-Vivo by Multiphoton Tomography—Variation with Depth and Correlation with Aging
    Cosmetics 2014, 1, 211-221; doi:10.3390/cosmetics1030211 OPEN ACCESS cosmetics ISSN 2079-9284 www.mdpi.com/journal/cosmetics Article Evaluation of Elastin/Collagen Content in Human Dermis in-Vivo by Multiphoton Tomography—Variation with Depth and Correlation with Aging Jean-Christophe Pittet 1,*, Olga Freis 2,†, Marie-Danielle Vazquez-Duchêne 2,†, Gilles Périé 2,† and Gilles Pauly 2,† 1 Orion Concept, 100 Rue de Suède, 37100 Tours, France 2 BASF Beauty Care Solutions France SAS, 3 Rue de Seichamps, CS 71040 Pulnoy, 54272 Essey-lès-Nancy Cedex, France; E-Mails: [email protected] (O.F.); [email protected] (M.-D.V.-D.); [email protected] (G.Pé.); [email protected] (G.Pa.) † These authors contributed equally to this work. * Author to whom correspondence should be addressed; E-Mail: [email protected]; Tel.: +33-247-052-316; Fax: +33-610-786-695. Received: 14 March 2014; in revised form: 31 July 2014 / Accepted: 1 August 2014 / Published: 20 August 2014 Abstract: The aim of this study was to evaluate the influence of the depth of the dermis on the measured collagen and elastin levels and to establish the correlation between the amount of these two extracellular matrix (ECM) components and age. Multiphoton Microscopy (MPM) that measures the autofluorescence (AF) and second harmonic generation (SHG) was used to quantify the levels of elastin and collagen and to determine the SAAID (SHG-to-AF Aging Index of Dermis) at two different skin depths. A 50 MHz ultrasound scanner was used for the calculation of the Sub Epidermal Non Echogenic Band (SENEB).
    [Show full text]
  • 06. Baransel Saygi
    Turkish Journal of Trauma & Emergency Surgery Ulus Travma Acil Cerrahi Derg 2008;14(2):103-109 The effect of dehydration and irrigation on the healing of Achilles tendon: an experimental study Dehidrasyon (kuruluk) ve irigasyonun (y›kama) Aflil tendon iyileflmesi üzerine etkileri: Deneysel çalıflma Baransel SA Y G I,1 Yakup YI L D I R I M,2 Cengiz ÇA B U K O ⁄ L U,3 Hasan KA R A,3 Saime Sezgin RA M A D A N,4 Tanıl ES E M E N L ‹ 5 BACKGROUND AMAÇ Air exposure is a factor that inhibits in vitro cellular prolifer- Hava teması tendonlarda canl›-d›fl› (in vitro) ortamda matriks ation and matrix synthesis in tendons. Aim of this experimen- sentezini ve hücre ilerlemesini azaltabilir ve hatta önleyebilir. tal study was to evaluate effect of dehydration and irrigation Bu çalıflmanın amacı, dehidrasyon ve irigasyonun Aflil tendon on healing of Achilles tendon. iyileflmesi üzerine etkisinin canl›-içi (in vivo) hayvan modeli METHODS üzerinde gösterilmesidir. Achilles tenotomy was done in forty-five Sprague-Dawley GEREÇ VE YÖNTEM rats. In control group, tendon was sutured immediately. In the K›rk befl adet Sprague-Dawley cinsi s›çan›n Aflil tenotomisi remaining two groups, the Achilles tendons were allowed to yapıldı. Kontrol grubunda, tendon hemen dikildi. Di¤er iki direct exposure of air. Irrigation of Achilles tendon was per- grubun cilt ve cilt altı dokuları ekarte edilerek Aflil tendon- formed in one of exposed groups, while irrigation was not larının do¤rudan hava ile teması sa¤landı. Bu gruplardan biri- done in other group.
    [Show full text]
  • Endotrophin Triggers Adipose Tissue Fibrosis and Metabolic Dysfunction
    ARTICLE Received 12 Sep 2013 | Accepted 21 Feb 2014 | Published 19 Mar 2014 DOI: 10.1038/ncomms4485 Endotrophin triggers adipose tissue fibrosis and metabolic dysfunction Kai Sun1,*, Jiyoung Park1,2,*, Olga T. Gupta1, William L. Holland1, Pernille Auerbach3, Ningyan Zhang4, Roberta Goncalves Marangoni5, Sarah M. Nicoloro6, Michael P. Czech6, John Varga5, Thorkil Ploug3, Zhiqiang An4 & Philipp E. Scherer1,7 We recently identified endotrophin as an adipokine with potent tumour-promoting effects. However, the direct effects of local accumulation of endotrophin in adipose tissue have not yet been studied. Here we use a doxycycline-inducible adipocyte-specific endotrophin overexpression model to demonstrate that endotrophin plays a pivotal role in shaping a metabolically unfavourable microenvironment in adipose tissue during consumption of a high-fat diet (HFD). Endotrophin serves as a powerful co-stimulator of pathologically relevant pathways within the ‘unhealthy’ adipose tissue milieu, triggering fibrosis and inflammation and ultimately leading to enhanced insulin resistance. We further demonstrate that blocking endotrophin with a neutralizing antibody ameliorates metabolically adverse effects and effectively reverses metabolic dysfunction induced during HFD exposure. Collectively, our findings demonstrate that endotrophin exerts a major influence in adipose tissue, eventually resulting in systemic elevation of pro-inflammatory cytokines and insulin resistance, and the results establish endotrophin as a potential target in the context of metabolism and cancer. 1 Touchstone Diabetes Center, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390, USA. 2 Department of Biological Sciences, School of Life Sciences, Ulsan National Institute of Science and Technology, 50 UNIST street, Ulsan 689-798, Korea.
    [Show full text]
  • Blood Vitronectin Is a Major Activator of LIF and IL-6 in the Brain Through Integrin–FAK and Upar Signaling Matthew P
    © 2018. Published by The Company of Biologists Ltd | Journal of Cell Science (2018) 131, jcs202580. doi:10.1242/jcs.202580 RESEARCH ARTICLE Blood vitronectin is a major activator of LIF and IL-6 in the brain through integrin–FAK and uPAR signaling Matthew P. Keasey1, Cuihong Jia1, Lylyan F. Pimentel1,2, Richard R. Sante1, Chiharu Lovins1 and Theo Hagg1,* ABSTRACT Microglia and astrocytes express the VTN receptors αvβ3 and α β We defined how blood-derived vitronectin (VTN) rapidly and potently v 5 integrin (Herrera-Molina et al., 2012; Kang et al., 2008; activates leukemia inhibitory factor (LIF) and pro-inflammatory Milner, 2009; Welser-Alves et al., 2011). Microglia and astrocytes, interleukin 6 (IL-6) in vitro and after vascular injury in the brain. as well as endothelial cells, are major producers of pro- α in vitro Treatment with VTN (but not fibrinogen, fibronectin, laminin-111 or inflammatory cytokines, such as IL-6 and TNF , and collagen-I) substantially increased LIF and IL-6 within 4 h in after traumatic or ischemic injury to the brain (Banner et al., 1997; C6-astroglioma cells, while VTN−/− mouse plasma was less effective Erta et al., 2012; Lau and Yu, 2001) or upon self-induction by IL-6 than that from wild-type mice. LIF and IL-6 were induced by (Van Wagoner and Benveniste, 1999). IL-6 is a major regulator of a intracerebral injection of recombinant human (rh)VTN in mice, but variety of inflammatory disorders and a target for therapies (Hunter induction seen upon intracerebral hemorrhage was less in VTN−/− and Jones, 2015).
    [Show full text]
  • With Caviar, Keratin & Collagen
    WITH CAVIAR, KERATIN & COLLAGEN Professional treatments for colour, bleaching, care and maintenance with CAVIAR, KERATIN and COLLAGEN Professional styling products with CAVIAR, KERATIN and COLLAGEN Technical professional products with CAVIAR, KERATIN and COLLAGEN 2 Professional products by Very high technology professional products to colour, treat and protect hair from the continuous chemical and environmental stress caused on a daily basis. Formulas based on: Caviar Keratin Collagen 3 WITH CAVIAR, KERATIN & COLLAGEN Colouring permanentCream professional ammonia PPD • Respects the hair structure thanks to an exposure free free time of 12 minutes • Non-progressive • Ammonia free • Paraphenylenediamine free • Unleashes all the EFFICANCY of its active principles and maximum COLOURING POWER Mix 1 : 1 4 WITH CAVIAR, KERATIN & COLLAGEN 1. Respect for scalp and hair thanks to a shorter processing time 2. Maximum grey hair coverage 3. Lightens up to 4 tones 4. Ammonia free and Paraphenylenediamine free 5. Safe application even on customers with a sensitive scalp 6. Extreme colour brilliancy and uniformity 7. Very easy and practical to use 8. Long lasting reflections 9. High colour fastness 10. Great protection action 11. Effective restructuring action benefits 12. Maximum conditioning 5 WITH CAVIAR, KERATIN & COLLAGEN Benefits 1 2 3 Respect for scalp and hair thanks to a shorter processing Lightens up to Maximum grey hair 4 tones time coverage 6 WITH CAVIAR, KERATIN & COLLAGEN has been developed according Cosmetic colour pDT BASE Be Colour 12 Minute Dpe DIAMINOPHENOXYETHANOL to the rules of the “molar stoichiometry,” a technique creamy gel with RESORCINOL m-AMINOPHENOL of colouring clear and uncompromising. It is based on CAVIAR, a mathematical principle according to which the molar concentration of the dye base is equal to the molar KERATIN and concentration of the sum of the other colouring couplers.
    [Show full text]
  • What Is Collagen?
    What is Collagen? Collagen is the most abundant protein in the human body and is as diverse as it is multifunctional (1). It is found throughout the body in a variety of forms and functions making up 30 percent of your body tissue and 70 % of your skin tissue. Specifically, collagen is the protein in connective tissue that is in bone marrow, tendons, cartilage, ligaments, and linings of your body organs. It is often referred to as the glue of the body. (1) Hydrolyzed collagen means the protein has been broken down into individual amino acids which are easier for the body to absorb. Collagen serves to help repair tissue and also functions in various roles throughout the body. Collagen and the Body Locations of Collagen: What Does Collagen Do? Collagen has numerous structural properties but also plays a vital role in the repair of almost all the body’s tissues. Some diseases are directly linked to lacking this essential protein. Depending on which part of the body it is located, collagen serves different purposes. In skin: Found in the inner layer, this connective tissue gives the skin its structure and strength and also functions in the replacement of dead skin cells. A lack of collagen in the skin can contribute to a decrease in skin health leading to stretch marks, dark spots, and infections as well as affecting the skin’s ability to maintain moisture. In internal organs and blood vessels: In the lining of your organs like in the stomach, kidneys, blood vessels and spleen, collagen functions as a protective covering and a fibrous barrier.
    [Show full text]
  • Fibrosis in Human Adipose Tissue
    ORIGINAL ARTICLE Fibrosis in Human Adipose Tissue: Composition, Distribution, and Link With Lipid Metabolism and Fat Mass Loss Adeline Divoux,1 Joan Tordjman,1 Danie`le Lacasa,2 Nicolas Veyrie,1,3 Danielle Hugol,1,4 Abdelhalim Aissat,1,3 Arnaud Basdevant,1,2 Miche`le Guerre-Millo,1 Christine Poitou,1,2 Jean-Daniel Zucker,1 Pierre Bedossa,1,5 and Karine Cle´ment1,2 OBJECTIVE—Fibrosis is a newly appreciated hallmark of the pathological alteration of human white adipose tissue (WAT). We investigated the composition of subcutaneous (scWAT) and hite adipose tissue (WAT) is the main energy omental WAT (oWAT) fibrosis in obesity and its relationship with repository in the body. It stores and mobi- metabolic alterations and surgery-induced weight loss. lizes, according to body demand, fatty acids RESEARCH DESIGN AND METHODS—Surgical biopsies for Wthat have been implicated in the development scWAT and oWAT were obtained in 65 obese (BMI 48.2 Ϯ 0.8 of insulin resistance. In turns, the phenotype and the kg/m2) and 9 lean subjects (BMI 22.8 Ϯ 0.7 kg/m2). Obese biology of WAT cellular components are altered by two subjects who were candidates for bariatric surgery were major processes: adipose cell hypertrophy and immune clinically characterized before, 3, 6, and 12 months after cells accumulation. Inflammation, reticulum endoplasmic surgery, including fat mass evaluation by dual energy X-ray stress, and hypoxia are part of the biologic alterations that absorptiometry. WAT fibrosis was quantified and character- ized using quantitative PCR, microscopic observation, and attract and retain inflammatory cells in WAT (1).
    [Show full text]
  • Empowering Collagen Targeting for Diagnosis and Treatment of Human Conditions
    EmpoweringEmpowering collagen collagen targetingtargeting for for diagnosis prognosis of fibrotic and treatment of Manka,SW. 2012 conditions.human conditions. 1 3Helix as a platform diagnostic company 2020 2022 2030 Innovative research reagent for Clinic histopathology providing Platform fibrotic prognostic detection of collagen damage best in class prognostic ability in within multi-disease states liver fibrosis (NAFLD, NASH) Strengthening IP portfolio with market Clinical histopathology AND Non-Invasive approaches serum testing and medical disrupting products while subsequently Analytic specific reagent to allow for fast imaging developing strong partnerships with world market access leading companies for commercialization Targeting impactful markets of IPF, kidney Focused on paired biopsy research and fibrosis, AMD, Keloids and cardiac fibrosis collaboration with clinical laboratories. in addition to fibrotic liver diseases. 2 Liver Fibrosis market is GROWING Fatty Liver Fibrotic Liver Healthy Liver Cirrhosis NAFLD NASH USA Epidemiology 328 Million 83 Million 16 Million 1.5 Million (2015) Predicted USA Epidemiology 360 Million 101 Million 27 Million 3.4 Million (2030) Estes,C. 2018 3 NASH Therapeutics are finishing clinical trials and are coming to market. • VK2809 Phase II • OCALIVA (OCA) • NDA Filed • $78,000/year current cost • $20,000 predicted • Resmetirom Phase III • 23% respond to treatment 16 Million NASH patients in the USA * $20,000 • $320 Billion Annual Cost for treatable market Aramchol Phase III/IV 4 Stratification of patient population is needed to reduce unnecessary therapeutic intervention. • Progression of NAFL and 100% NASH is variable patient to NAFLD patient. 33% • Prediction of the progression can modify the Fibrosis Progression 20% disease intervention and treatment. Rapid Fibrosis • No product on the market Progression (stage 0 to stage today is equipped for 3/4 over 5.9 years) prognosis of liver fibrosis Singh, S.
    [Show full text]
  • Skeletal Muscle – Fibrosis
    Skeletal Muscle – Fibrosis Figure Legend: Figure 1 Skeletal muscle - Fibrosis in a male Harlan Sprague-Dawley rat from a subchronic study. Early change consists of increased perimysial deposits of pale eosinophilic material (immature collagen). Figure 2 Skeletal muscle - Fibrosis in a male Harlan Sprague-Dawley rat from a subchronic study. Note the perimysial proliferation of fibroblasts and early collagen deposition. Figure 3 Skeletal muscle - Fibrosis in a male Harlan Sprague-Dawley rat from a subchronic study (higher magnification of Figure 2). There is deposition of perimysial connective tissue and attenuation of several muscle fibers. Figure 4 Skeletal muscle - Fibrosis in a male F344/N rat from a chronic study. There is marked fibrosis with attenuation and loss of muscle bundles. 1 Skeletal Muscle – Fibrosis Comment: In skeletal muscle, the predominant histologic features of fibrosis are increased numbers of plump reactive fibroblasts with prominent vesiculated nuclei, and increased amounts of pale eosinophilic fibrillar material (collagen deposition) separating and surrounding adjacent myofibers (Figure 1, Figure 2, Figure 3, and Figure 4). Affected myofibers may or may not exhibit histologic features of atrophy, degeneration, necrosis, or regeneration. Fibrosis is the end result of a cascade of events that begins with tissue injury and inflammation and ends in permanent scar formation. When tissue is damaged, profibrotic cytokines, such as transforming growth factor beta, are released by the infiltrating inflammatory cells. These cytokines signal the fibroblasts to migrate into the affected region and to begin producing and remodeling the extracellular matrix. The stromal fibroblasts then begin producing cytokines, growth factors, and proteases that further trigger and uphold the inflammatory/profibrotic conditions.
    [Show full text]
  • Deciphering the Cellular Interplays Underlying Obesity-Induced Adipose Tissue Fibrosis
    Deciphering the cellular interplays underlying obesity-induced adipose tissue fibrosis Geneviève Marcelin, … , Adaliene V.M. Ferreira, Karine Clément J Clin Invest. 2019. https://doi.org/10.1172/JCI129192. Review Series Obesity originates from an imbalance between caloric intake and energy expenditure that promotes adipose tissue expansion, which is necessary to buffer nutrient excess. Patients with higher visceral fat mass are at a higher risk of developing severe complications such as type 2 diabetes and cardiovascular and liver diseases. However, increased fat mass does not fully explain obesity’s propensity to promote metabolic diseases. With chronic obesity, adipose tissue undergoes major remodeling, which can ultimately result in unresolved chronic inflammation leading to fibrosis accumulation. These features drive local tissue damage and initiate and/or maintain multiorgan dysfunction. Here, we review the current understanding of adipose tissue remodeling with a focus on obesity-induced adipose tissue fibrosis and its relevance to clinical manifestations. Find the latest version: https://jci.me/129192/pdf The Journal of Clinical Investigation REVIEW SERIES: MECHANISMS UNDERLYING THE METABOLIC SYNDROME Series Editor: Philipp E. Scherer Deciphering the cellular interplays underlying obesity- induced adipose tissue fibrosis Geneviève Marcelin,1 Ana Letícia M. Silveira,1,2 Laís Bhering Martins,1,2 Adaliene V.M. Ferreira,2 and Karine Clément1,3 1Nutrition and Obesities: Systemic Approaches (NutriOmics, UMRS U1269), INSERM, Sorbonne Université, Paris, France. 2Immunometabolism, Department of Nutrition, Nursing School, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. 3Nutrition Department, Hôpital Pitié-Salpêtrière, Assistance Publique Hôpitaux de Paris, Paris, France. Obesity originates from an imbalance between caloric intake and energy expenditure that promotes adipose tissue expansion, which is necessary to buffer nutrient excess.
    [Show full text]
  • Fibrotix: Significant Reduction in Skin Scar Area, Fibrosis, Hyperpigmentation and Improved Appearance
    Fibrotix: Significant Reduction in Skin Scar Area, Fibrosis, Hyperpigmentation and Improved Appearance Challenge • Wound healing is complex: excessive inflammation, angiogenesis and dermal fibroblast function significantly contribute to scarring; additionally, scar hyperpigmentation negatively impacts scar quality · Reduces skin scar area • Scars cause serious cosmetic and functional problems that can be emotionally and physically debilitating and place and hyperpigmentation heavy financial burdens on healthcare systems post wound in vivo • There are currently no clinically tested or licensed · Uses Salbutamol a safe, interventions/pharmaceuticals available to reduce scarring or widely used, approved scar hyperpigmentation therapeutic · Strong intellectual Solution property position • Salbutamol (Sal), delivered topically, ameliorates excess deposition of scar tissue and reduces hyperpigmentation post trauma, significantly improving scar appearance www.le.ac.uk/business Fibrotix: Significant Reduction in Skin Scar Area, Fibrosis, Hyperpigmentation and Improved Appearance Macroscopic scar assessment at 56 days post wounding figure 1 Using a number of in vitro and in vivo models we have Salbutamol reduces scar area at 28, 42 and 56 days post wounding demonstrated that Sal-induced beta 2 adrenoceptor activation can restrain inflammation, angiogenesis and dermal fibroblast differentiation, function and pro- fibrotic signature via a number of mechanisms. In vivo proof-of-principle studies were performed in the Red Duroc pig and demonstrated Sal treatment reduced scar area by almost 50%, 56 days post-wounding. Hyperpigmentation, colour match, sheen, height, texture and pliability were also significantly improved (figure 1). Market Immunostaining demonstrated a significant early 100 million patients in the developed world heal with a scar reduction in both macrophage infiltration and every year as a result of elective procedures and trauma.
    [Show full text]