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Boston Professional Events List
10th Diabetes Drug Discovery & Developmental Conference.
Apr 26, 2017 - 07:00 AM - Apr 27, 05:30 PM
Hyatt Regency Boston 1 Ave de Lafayette, Boston, MA 02111,
Experts from industry and academia will discuss the bionic pancreas, bariatric surgery, the gut microbiome, obesity, and emerging therapies to target Type 1 and Type 2 diabetes in sessions and panels geared towards novel therapeutic treatments, strategies, and drug discovery at the 10th Diabetes Drug Discovery & Developmental Conference.
This conference is part of the 2017 Diabetes Summit taking place April 26-27, 2017 in Boston, MAand encompasses the drug discovery and partnering aspects of diabetes in two individual conferences that take place concurrently:
10th Diabetes Drug Discovery & Development Conference
7th Diabetes Partnering & Deal-Making Conference
We hope to see you there!
The 2017 Advisory Committee
|2016 GOLD SPONSORS|
|2016 CORPORATE SPONSORS|
|2016 MEDIA PARTNERS|
|Day 1 - Monday, April 25, 2016|
|7:00||Registration & Continental Breakfast|
|7:55||Welcome & Opening Remarks|
|New Discoveries and Emerging Therapies for Type 1 Diabetes
Moderator: Corinth Auld, Mercodia
|8:00||Global Clinical Trial Updates on BCG Vaccinations for the Treatment and Reversal of Autoimmunity|
Director and Associate Professor of Medicine
Massachusetts General Hospital
Harvard Medical School
|The bacillus Calmette-Guerin (BCG) vaccine—first used over 100 years ago for tuberculosis prevention—represents the most continuously used and safest vaccine in world history. Currently, there are 10 human clinical trial testing repeat BCG vaccination in diverse forms of autoimmunity and allergies around the globe, both for prevention of these conditions as well as for treatment (including both new onset and longstanding conditions). A Phase I study of the BCG vaccine in longstanding type 1 diabetes (T1D) reveals potential disease modulating effects after repeated BCG vaccination, including death of autoreactive cells, transient and modest restoration of insulin secretion and induction of beneficial regulatory T cells (Tregs). A Phase II clinical trial using multi-dose BCG in longstanding T1D was initiated in June 2015. The double-blinded, placebo controlled trial protocol is unique in testing the efficacy of the BCG vaccine in long-term diabetic subjects (average disease duration: 15-20 years) with small but detectable levels of C-peptide secretion from the pancreas. Based on published Phase II clinical trial data of BCG in multiple sclerosis subjects, the therapeutic effects of this vaccine appear to improve over the passage of time; therefore, potential clinical benefits in the diabetes trial will be followed for 5 years. The primary endpoint is decrease in HbA1c in treated vs placebo subjects. The selection of BCG as an immune intervention in T1D is based on the protective host TNF response, including induction of Tregs, and potential long-term modulation of the immuno-inflammatory profile of vaccinated subjects.|
|8:25||Islet Regeneration: Highest Unmet clinical Need Among all Metabolic Diseases: Progress Report|
President and CEO
|A wide spectrum of therapeutic modalities are targeted at relieving the insulin-dependent person of the unremitting threat of serious hypoglycemia and diabetic complications. The “artificial pancreas” and encapsulated islets have good prospects of reducing this threat and the risk of complications in the near term. A gene therapy may ultimately provide the definitive approach but no practical genetic approach is on the horizon. Islet regeneration (IR) almost certainly occurs throughout life in nondiabetic people and even in people with longstanding T1D. Some evidence suggests that IR can be pharmacologically induced. If so, an effective IR agent could actually reverse both forms of diabetes, assuming that T1D autoimmunity and insulin resistance can be controlled. A prototypical combination therapy clinical study is underway right now. Positive results should encourage further efforts at developing disease modifying combinations of IR and immunomodulatory agents for people with T1D.
Benefits of this talk include an improved understanding of
• The ecology of approaches aimed at “practical cures” of T1D
• Evidence that supports islet regeneration can be induced in people with diabetes
• Why it is relatively easy to know when islet regeneration has been induced.
• Why inducing islet regeneration is the only foreseeable approach for reversing both types of diabetes
• Distinctive clinical trial design and regulatory considerations for developing IR therapies for T1D
|8:50||The Long and Winding Road to the Bionic Pancreas|
|Edward R. Damiano
Professor of Biomedical Engineering
Assistant Professor of Medicine
Massachusetts General Hospital
Harvard Medical School
|9:40||Oral Presentation: Generation of Fully Functional Islet-like Structures from Adult Human Liver Stem Cells|
Director, Regenerative Medicine, Global Research and Development
Fresenius Medical Care Deutschland GmbH
Senior Executive Manager, StemCell Project , Chief Scientific Officer
|Both pancreas and islet transplantation have been shown to restore islets function and potentially reduce long-term diabetic complications, but are limited by both donor shortage and need for immunosuppression. Stem cells represent a promising source for the generation of insulin-producing cells for the cure of type 1 diabetes mellitus (T1DM). Adult Human Liver Stem Cells (HLSC) are easily obtained and expanded from a small liver biopsy of adult subjects. Furthermore, they express a number of stem cells and embryonic markers and have been shown to differentiate, in vitro, into islet-like structures (HLSC-ILS). HLSC are currently GMP-produced and they exhibit a significant immunosuppressive action. The aim of the present study was to develop a simple and reproducible one-step differentiation protocol for scalable production of functional HLSC-ILS. Results: with the aid of polycationic molecules, HLSC undergo differentiation into 3D spheroid structures resembling human islets for both size and cellular composition (protein expression of insulin/C-peptide, glucagon, somatostatin, ghrelin, pancreatic polypeptide and Glut-2). Such structures, in vitro, produce C-peptide after stimulation with high glucose and, in vivo, following their implant under the renal capsule of streptozotocin-induced diabetic SCID mice, significantly reduce glycemic levels. In conclusion, HLSC may undergo functional HLSC-ILS differentiation, thus representing a potential stem cells source for the cure of diabetes.|
|10:00||Morning Networking Break|
|New Discoveries and Treatment for Type 2 Diabetes
Moderator: Harith Rajagopalan, Founder and CEO, Fractyl Laboratories
|10:45||Fibroblast Activating Protein as a New Target for the Treatment of Type-2 Diabetes|
Tufts University School of Medicine
|Fibroblast activating protein is sequentially and structurally very similar to dipeptidyl amino peptidase type 4 (DPP4), a post proline cleaving serine protease that is now a validated target for type 2 diabetes. FAP’s substrate specificity strongly overlaps with that of DPP4 although it ability to cleave DPP4 substrates such as GLP-1 does not seem to be biologically relevant. FAP’s expression profile is quite different from that of DPP4. It is found in lower amounts in the blood and throughout the body than DPP4, which may explain the irrelevance of its ability to cleave GLP-1 and other DPP4 substrates. Recently, FAP has recently been reported to cleave and limit the circulating lifetime of human, but not mouse FGF-21, suggesting that FAP inhibitors might have anti diabetic activity in humans, even if perhaps not in mice. However, an FAP knockout mice has been reported to have improved glucose tolerance, resistance to diet induced obesity and resistance to dyslipidemia, suggesting that FAP must be limiting the lifetimes of peptides with anti diabetic activities in addition to human FGF-21, thereby further implicating FAP as a potential target for Type 2 diabetes. This talk will review and critically evaluate the existing evidence implicating FAP as a target for treating type-2 diabetes, present some preliminary results on the effects of specific and potent inhibition of FAP in mice and discuss potential substrates of FAP that may be mediating the anti-diabetic activity.|
|11:20||Challenging the Status Quo: Unleashing Disruptive Innovation|
President, Chief Operating Officer and Chairman
|Intarcia Therapeutics, Inc. is developing innovative therapies that merge medicine and technology to transform the lives of patients suffering from chronic diseases. Intarcia's platform technology allows the stabilization of proteins and peptides at above-body temperature and extended delivery in a consistent and continuous manner through a proprietary osmotic mini-pump which is placed just under the skin just once or twice yearly. The lead compound, ITCA 650 (continuous SC delivery of exenatide), is currently being evaluated for type 2 diabetes (T2D) in the FREEDOM Phase 3 clinical program. The product pipeline is focused on “next gen” diabetes, obesity and anti-inflammatory conditions.
Despite >40 pills and injections launched into the diabetes market in the past decade, T2D trends have not improved and T2D continues to be a worldwide killer with one person dying every 6 seconds and >50% of patients are not at HbA1c goal over time. Pills and injectables have an alarming rate of poor adherence and persistence with 3 out of 4 patients stopping their T2D treatment every year. Available agents are failing to get and keep many patients at HbA1C goal over time. Instead of yet another pill or injection, it is time to find innovative new solutions. ITCA 650 is one promising and highly innovative solution designed to finally change the treatment paradigm and address the key unmet needs in T2D.
Over 5200 patients have participated in the FREEDOM program. Both FREEDOM-1 and FREEDOM-1 HBL, presented at ADA and EASD 2015, demonstrated significant and clinically meaningful reductions in HbA1C, weight reduction, and percent of patients treated to goal. In FREEDOM-1, patients primarily on background metformin or diet and exercise treated with ITCA 650 60 mcg/day achieved a mean HbA1C reduction of 1.7% and 4kg weight loss at week 39. In FREEDOM-1 HBL, difficult to treat patients with an initial high baseline HbA1C (mean, 10.8%), achieved a mean reduction in HbA1C of 3.4% at week 39. In the latest trial, FREEDOM-2, ITCA 650 demonstrated head-to-head superiority in HbA1C control and weight loss after 52 weeks over the market-leading oral therapy, Januvia® (sitagliptin). Patients in the ITCA 650 arm had twice the A1C reduction and three times the weight loss as those in the Januvia arm."
Founder and CEO
|12:25||Lunch provided by GTCbio|
|1:30||The Candidate Drug CS6253 is an ABCA1 Agonist with Anti-diabetic and Atherosclerosis Reduction Actions|
President & CEO
|Background: Current Type 2 Diabetes Mellitus (T2DM) medicines do not impact atherosclerosis and cardiovascular disease (CVD) risk, the main cause of morbidity and death. CS6253 is a 2nd generation selective ABCA1 agonist that is potent, drugable and safe.
Methods: In vitro and in vivo studies were carried out in lipoprotein transport - atherosclerosis and glucose metabolism - diabetes models to assess the therapeutic potential of CS6253 in T2DM.
Results: The ABCA1 cholesterol efflux potency of CS6253 approximated that of apoA-I and apoE on a molar basis. CS6253 single injection increased macrophage specific reverse cholesterol transport for 24 hours in apoE KO mice illustrating the long functional half-life. ApoE KO mice given Western diet for 14 weeks and then treated for 6-10 weeks, 10-30mg/kg/48h, showed significant atherosclerosis reduction in dose-dependent manner (p<0.01 vs. control).
CS6253 stimulated insulin secretion and insulin sensitivity in state of the art cell models, i.e. INS-1 823/13 and L6-Glut4myc rat myoblasts.
Diet Induced Obesity (DIO) mice were treated with CS6253 30mg/kg sc alternate days or PBS control for 16 weeks. Glucose Tolerance Testing (GTT) was improved already after 5 weeks treatment consistent with the observed increase in glucose mediated insulin secretion with additional improvement over 16 weeks’ time suggestive of insulin sensitizing effects. Ob/ob mice treatment results with the ABCA1 agonist were consistent with the DIO findings.
Discussion: The dual atherosclerosis-reduction and anti-diabetic actions of the candidate drug CS6253’s suggest utility in the treatments of CVD in T2DM and/or T2DM in high risk CVD patients.
Talk-Benefits; New target, unmet medical need, candidate drug
Director of Research
|2:20||Autologous Polyclonal Ex-Vivo Expanded Treg Therapy for New Onset Type 1 Diabetes in Children|
Chief Medical Officer
|T1DM in children is characterized by increased immune activation and a more aggressive clinical course compared to the adult population. Mounting evidence suggests that adoptive transfer of regulatory T-cells (Tregs) can slow disease progression and potentially lead to remission. Previous phase 1 clinical trials have demonstrated that expanded polyclonal Tregs are safe and well tolerated in both adults and children, supporting the development of a phase 2 trial to assess safety and efficacy of Treg therapy for T1DM in adolescents.
Caladrius Biosciences has launched a phase 2, double-blind, placebo-controlled, multi-center exploratory trial to assess the safety and efficacy of autologous Tregs to modify the T1DM disease course, including preservation of β-cell function and improvements in disease severity in adolescents (aged 12 to 17 years) with recent onset T1DM.
Approximately 111 subjects will be randomized to one of 3 treatment groups in a 1:1:1 ratio (placebo, 2.5 or 20 million Treg cells/kg BW). Key endpoints include the 2-hour and 4-hour Mixed Meal Tolerance Test (MMTT) stimulated C-peptide AUC at various time points through 24 months, daily dose of insulin use, severe hypoglycemia, and the percentage of subjects achieving partial or complete T1DM remission. Subjects will be followed for 2 years. A safety review will be conducted after the initial 18 subjects have been randomized and followed for 3 months. An interim analysis is planned after approximately 50% of subjects complete the Week 26 visit.
This phase 2 study will advance insight into the safety and potential efficacy of adoptive transfer of Tregs to modify the T1DM disease course in adolescents with recent onset T1DM as well as providing unprecedented insights into immune regulatory function.
Emeritus Professor of Pharmacy, Chief Science Officer
University at Buffalo, Volant Pharma A.G.
|3:10||Afternoon Networking Break|
Co-Founder, President, Chief Scientific Officer and Board Director
|Advances and Strategies in Drug Development|
Investigator, Genetics of Development and Disease Branch
|4:30||Pre-clinical Characterization, Toxicological and Safety Assessments of MOD-6031- A Novel Long-Acting Dual GLP-1/Glucagon Agonist, Supports Phase I Study Initiation in Over Weight and Obese Healthy Subjects|
General Manager, R&D
OPKO Biologics Ltd. (f.k.a. Prolor-Biotech Ltd.)
*Overview of non-clinical development of a long-acting GLP-1R/GCCR agonist
*hear about the pharmacological activity of Oxyntomodulin
*learn about Phase 1 design to assess safety but aslo pharmacological aspects of Oxyntomodulin
Pre-clinical Characterization, Toxicological and Safety assessments of MOD-6031-
a Novel Long-Acting Dual GLP-1/Glucagon Agonist, supports Phase I Study Initiation in Over Weight and Obese Healthy Subjects
L. Israeli-Yagev2, A. Bar-Ilan 2, V. Lev 1, G. Hart 2, O. Hershkovitz 1
1CMC 2R&D, OPKO Biologics, Nes Ziona, Israel
MOD-6031 is a novel long acting dual GLP-1/Glucagon agonist developed by OPKO Biologics for the indication of weight management and potentially type 2 diabetes. It is comprised of a 37 amino acid synthetic Oxyntomodulin (OXM) peptide, identical in sequence to the endogenous human OXM, conjugated to polyethylene glycol (PEG) via a hydrolysable linker that spontaneously hydrolyzes under physiological conditions. This technology enables a slow and controllable release of the intact OXM and substantially prolong its exposure and, consequently improves its potential to interact with its target receptors, GLP-1 and Glucagon, and cross the blood-brain barrier.
The extended half live of OXM (from ~10 min to ~9 hr) and its pharmacological efficacy were confirmed in vitro and in several species and diabetes/obesity models following MOD-6031 subcutaneous administration. Remarked induced weight loss and food intake inhibition were observed, as well as significant improvement of the glycemic and lipid profiles. A battery of comprehensive toxicological and safety pharmacological studies demonstrated an excellent safety profile without any unexpected adverse events at significant margins above the clinical doses. The changes noted were related to an exaggerated pharmacological response to the drug’s weight loss effect at the high doses. No antibodies to MOD-6031 were detected.
The enhanced exposures and half-life of hydrolyzed OXM, together with the safety profile of MOD-6031, support the initiation of Phase Ia study, designed to assess the safety, tolerability and pharmacokinetics of MOD-6031 in healthy overweight or obese subjects, receiving single escalating doses, in a placebo-controlled design. Exploratory pharmacodynamic responses will be evaluated by monitoring glucose, insulin, FFA, Triglycerides and Adiponectin blood levels and by monitoring glucose levels following a Mix Meal Tolerance Test.
|4:55||Day 1 Concludes|
|Day 2 - Tuesday, April 26, 2016|
|Joint Session with Stem Cell Research in the Diabetes Space
Moderator: Kevin A. D'Amour, Viacyte
|8:00||Biologic Replacement and Regenerative Medicine Strategies for Diabetes|
Stacy Joy Goodman Prof. of Surgery; Distinguished Prof. of Medicine; Prof. of Biomedical Engineering, Microbiology and Immunology; Director, Diabetes Research Institute and Cell Transplant Program
University of Miami
|Strategies aimed at restoring beta cell mass generally fall under either Replacement (islet transplantation and stem cell differentiation), Reprogramming (from non-insulin-producing cells) or Regeneration (replication and induction from endogenous precursors/stem cells).
Objectives of cellular therapies and regenerative medicine strategies for treatment of DM are to reverse the disease condition and prevent the development of the severe chronic complications that can affect most organ systems in a large proportion of patients over time.
A multicenter Phase III trial of transplantation of adult pancreatic islet has been recently completed and is moving towards a Biological License Application (BLA) in the USA, while novel strategies to engineer an intra-abdominal mini-endocrine pancreas are currently tested in pilot clinical trials.
In T1DM, the additional challenge of the underlying autoimmune condition imposes consideration of strategies that would restore self-tolerance or abrogate the effects of autoimmunity, so that the immune system can no longer destroy the new insulin producing cells introduced either by regenerating, reprogramming or replacement (e.g., transplantation of pancreatic islets or stem cell derived insulin producing cells). Abrogation of autoimmunity or its effects could be achieved by either tolerance induction strategies or immune protection (e.g., engineered microenvironment or selective permeability physical barriers like those introduced by micro-, conformal- or nano-encapsulation). Any therapeutic strategy, to be considered must avoid side effects such as those associated with life-long immunosuppression, which now limits the indications of adult islet transplantation to the most severe cases of T1DM. There is a broad consensus on the idea that stem cells will eventually replace adult pancreatic islets in the future. However, the jury is still out regarding the candidate cell type/s and approach that will ultimately succeed. Current differentiation methods for adult stem cells span from signal-driven approaches, to genetic manipulation and even strategies of in-vivo maturation after systemic administration. The more suitable alternatives between replacement, reprogramming and regeneration strategies should be further developed in pre-clinical model systems and tested in pilot clinical trials, while carefully assessing safety, efficacy, cost-effectiveness and the relative potential for scale up, to offer a realistic therapeutic option for most patients affected by diabetes.
|8:45||The Challenge of Stem Cells Research; Many Hurdles Remain|
Faculty Member, Medicine - Diabetes Division
University of Texas Health Science Center at San Antonio
|The quest to replace insulin injection treatment has focused on two strategies: in vivo islet transplantation and in vitro nuclear reprogramming to produce differentiated beta cells. Ultimately, both strategies rely on encapsulation to implant islets or culture cells into the human body. The many hurdles involved with islet transplantation have yet to be overcome and, even if successful, the paucity of pancreatic donors limits this approach. An alternative approach has attempted to recapitulate the embryonic development of pancreatic beta cell in vitro using stem cells. However, the stem cell approach requires in vitro cell culture and still has to overcome the hurdle of encapsulation. Beyond the capsulation hurdle, there remains a lack of knowledge about the basic molecular/cellular events via which a completely undifferentiated cell can be transformed into a functioning tissues/organ which can be integrated into whole body homeostasis. Mark Twain said: “What gets us into trouble is not what we don’t know, it’s what we know for sure that just ain’t so.|
|9:15||Development of Stem-Cell Derived, Macroencapsulated Islet Replacement for Type 1 Diabetes|
|Kevin A. D'Amour
Vice President, Research
Chief Scientific Officer
|ViaCyte Inc. is a clinical stage company developing a stem cell-based islet replacement therapy for treatment of patients with diabetes. The therapy is a combination product comprised of pancreatic endoderm cells encapsulated within a retrievable delivery device, ENCAPTRA® Drug Delivery System. After implantation, encapsulated progenitor cells differentiate into glucose-responsive, insulin-secreting cells. The renewable starting material for cell product manufacturing is human embryonic stem cells that are directed to differentiate to the pancreatic endoderm cell product using scalable processes. The bio-stable delivery device is designed to fully contain cells and to protect cells from immune attack, with the goal of eliminating the need for immunosuppressant drugs.
Funding in part from California Institute for Regenerative Medicine; SP1-06513, DR1-01423, TR1-01215 and JDRF.
|9:45||Combinatorial Development of Materials for Islet Transplantation|
|Daniel G. Anderson
Massachusetts Institute of Technology
|The fibrotic reaction to implanted biomaterials is a fundamental challenge to the development of immuno-isolation devices. Here we describe our work developing new biomaterials and devices for the purposes of enabling islet transplantation. In particular we describe the development of a large library of synthetic hydrogel materials, and the characterization of their biocompatibility in vivo. Data will be presented on the nature of the immune response to these and conventional biomaterials. Several lead materials have been identified with significantly improved biocompatibility in rodents and primates. When formulated into microcapsules these materials enable functional, long-term islet transplantation in immune competent, diabetic rodents.|
|10:15||Morning Networking Break|
|Novel Therapeutic Targets & Strategies for Diabetes Treatment
Moderator: Dan Grau, Heptares Therapeutics
|10:45||Novel Therapeutic Targets & Strategies for Diabetic Foot Ulceration and Peripheral Neuropathy|
Beth Israel Deaconess Medical Center
|Fifteen percent of diabetic patients are expected to develop diabetic foot ulceration (DFU) within their lifetime. With the expected increase of incidence of diabetes, DFUs will represent an even bigger burden for the healthcare system of both developed and developing countries and may prove to be one of the most costly complications of diabetes. Although there is some overlap, acute normal wound healing can be divided in three phases: coagulation-inflammation, proliferation and remodeling. Chronic wounds, like the DFU, lack this linear progression from one phase to the next and are mainly characterized by the persistence of the inflammatory phase, although progression to the proliferation phase may be present in certain wound areas. Substance P and mast cells (MC) are involved in different phases of wound healing. Diabetes and the associated SP deficiency are associated with an absence of an acute inflammatory response important for wound healing progression and cause a persistent inflammation through all the healing process. SP treatment induces an acute inflammatory response which enables the progression to the proliferative phase and modulates macrophage activation towards the M2 phenotype that promotes wound healing. In addition, the number of degranulated MCs is increased in unwounded forearm and foot skin of DM patients, and unwounded dorsal skin of DM mice. Conversely, post-wounding MC degranulation increased in non-DM but not in DM mice. Pre- and post- wounding mice treatment with MC stabilizers rescues the DM-associated wound healing impairment in mice and shifts macrophages to the regenerative M2 phenotype.|
|11:10||Opportunities to Restore Beta Cell Function in Diabetes|
Professor of Medicine
Joslin Diabetes Center
Harvard Medical School
|Insufficient insulin secretion is fundamental to the pathogenesis of both types 1 and 2 diabetes. The amount of insulin secreted depends upon the mass or number of beta cells and the function of those cells. It is now becoming apparent that there is a slow turnover of beta cells throughout life such that existing beta cells replicate and new islets are formed. There continues to be hope that beta cells can be regenerated, but the promising results in rodents with GLP-1 agonists have not been apparent in humans over the past decade.
While the prospects for eventual success with beta cell replacement by transplantation and even regeneration are promising, restoration of beta cell function should be a major therapeutic priority. Beta cells in diabetes can lose as much as 70% of their function, mainly through glucose toxicity. There is every reason to think that this function can be restored by blood glucose control obtained with interventions including lifestyle changes, drugs and bariatric surgery.
Professor, Department of Biological Chemistry & Molecular Pharmacology
Joslin Diabetes Center
|12:00||Inflammation-resolving Lipid Mediators in Diabetic Wound Healing and Ischemic Revascularization|
Assistant Professor, Center for Experimental Therapeutics and Reperfusion Injury
Harvard Medical School and Brigham and Women's Hospital
|Tissue injury arising from trauma, surgery or ischemia elicits a prompt inflammatory response. A primary goal of the inflammatory response is to eliminate exogenous pathogens and to promote the clearance of dead cells. Timely resolution of the inflammatory phase enables the transition from inflammation to tissue repair, whereas chronic unresolved inflammation in diabetes perturbs tissue repair. Resolvins are a family of lipid mediators that promote resolution of inflammation by decreasing neutrophil trafficking and promoting macrophage-mediated clearance of bacteria and dead cells. This presentation will provide an overview of resolvin biosynthesis and highlight our recent work showing that resolvins promote wound healing and tissue revascularization in diabetes. The ultimate goal of our research is to understand how the resolution phase of inflammation is linked to tissue repair in order to develop novel therapeutics for resolving chronic inflammation and promoting host defense and tissue repair.|
|1:45||6th Diabetes Partnering & Deal Making Conference Begins|
Keywords: conference , development , industry , Treatment, conference , Conference , Conferences , Develop , development , industry
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