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Dr. Paul Fernyhough

Dr. Paul Fernyhough

Division of Neurodegenerative Disorders

Principal Investigator,
Cell Biology of Neurodegeneration Lab, Division of Neurodegenerative Disorders

Pharmacology and Therapeutics, Max Rady College of Medicine
Rady Faculty of Health Sciences, University of Manitoba

WinSanTor Inc.

Research Focus

The WHO informs us that by 2025 there will be 300 million sufferers from diabetes worldwide – a figure approximately equal to the population of the USA. Neurobiologist Dr. Fernyhough is studying the etiology of the peripheral nerve damage observed in patients with diabetes. In addition, he is researching the link between Alzheimer’s disease and Type 2 diabetes. “In patients with Alzheimer’s disease there is an increased risk of developing diabetes and these patients exhibit more severe and accelerated memory loss,” says Dr. Fernyhough. Our studies are focused on identifying key signalling pathways that are impaired in animal models of Alzheimer’s disease. A major direction of the lab is to determine whether improper insulin signal transduction in neurons is central to the axon and neuronal loss. 

Abnormal peripheral nerve function in diabetic neuropathy

Evidence of neurodegenerative disease has been found in the peripheral nervous system in diabetes – commonly called diabetic neuropathies that involve damage to peripheral sensory neurons. Currently close to 50% of diabetic patients develop some form of peripheral nerve disease, which can lead to loss of protective sensation and limb amputation. The Aboriginal populations of Canada and the USA are experiencing an explosion in the incidence of type 2 diabetes. The incidence is expected to rise 10-fold in the next 10 years in First Nations peoples of Canada. Manitoba has one of the largest numbers of Aboriginal persons in Canada and so the health burden in this province is becoming severe. Diabetic sensory neuropathy and retinopathy are particularly severe complications in these populations. Approximate direct health costs in Manitoba for neuropathy (including amputation and foot treatment) are CA$100-150 million per annum. This excludes the social costs of loss of work, relocation and rehabilitation. The human cost is enormous. Young patients, 30 years of age, are undergoing amputations and death from infection is increasingly occurring.

Why is this work important?

Currently, there are no effective treatments for any of these serious neurological diseases. Dr. Fernyhough’s research is focused on identifying the key cellular/molecular pathways that are regulated by insulin in the maintenance of mitochondrial function and determining what goes wrong in diabetic sensory neuropathy and Alzheimer’s disease.

What techniques and equipment are used in this laboratory?

  • In vitro and in vivo models
  • Animal models of type 1 and 2 diabetes (STZ rat and mouse; ZDF rat)
  • Primary sensory neuron cell culture
  • Molecular studies
  • Confocal microscopy – inverted and upright
  • Real time video microscopy – calcium, mitochondrial function, free radicals (standard light and confocal – Zeiss LSM 510)
  • In vitro enzyme assays
  • Viral-mediated transfection – lentivirus and adenovirus
  • Western and Northern blotting (quantitative)
  • Real time RT-PCR

The Division of Neurodegenerative Disorders (DND) occupies 5,000 square feet of newly-renovated laboratory space. This includes; laboratories for six principal investigators (2 new PIs to be hired in the next year), three culture rooms, a major equipment room, a Carl Zeiss LSM510 confocal microscopy room, a room for calcium imaging, a Carl Zeiss Axioskop II light upright microscope suite, a Bio-Rad Fluor-S imaging suite, HPLC room, a dark room, a walk-in cold room, two non-human surgery and behavioural monitoring rooms, and a conference/student room.

About Dr. Paul Fernyhough

Dr. Fernyhough was born and educated in East London, UK, and performed his B.Sc. degree in Biological Sciences at the University of Essex. Dr. Fernyhough performed his Ph.D. in biochemistry in the Department of Biochemistry at the University of Sheffield in the UK. He also performed postdoctoral research at Colorado State University, Kings College London and as a Wellcome Trust Postdoctoral Fellow at St Bartholomew’s Medical College. All of these positions spanned 1985-1998. Dr. Fernyhough subsequently worked for 5½ years (1998-2004) as a fully tenured lecturer in the School of Biological Sciences (now the Faculty of Life Sciences) at the University of Manchester. Dr. Fernyhough’s general research interest is in the cell biology underlying neurodegenerative disorders of the peripheral and central nervous systems.

For more information, please contact:

Dr. Paul Fernyhough
Director – Division of Neurodegenerative Disorders at the St. Boniface Hospital Research Centre &
Professor, Dept. of Pharmacology & Therapeutics, University of Manitoba, Faculty of Medicine

Room R4046, 351 Tache Avenue
Winnipeg, Manitoba, Canada
R2H 2A6

Phone: (204) 235-3939
Fax: (204) 237-4092

Muscarinic receptor antagonism as a novel mechanism for sensory nerve repair (CIHR)

Diabetic sensory neuropathy and chemotherapy-induced peripheral neuropathy (CIPN) are neurodegenerative diseases characterized by loss of nerve fibres in the skin. Both diseases cause significant pain and eventually lead to sensory loss. The impact of these diseases on human health is enormously damaging and there are no therapies. Our recent work has uncovered an endogenous signalling pathway in neurons that negatively modulates nerve fibre growth of sensory neurons. The neurotransmitter, acetylcholine, is produced by sensory neurons and skin cells and activates the muscarinic receptor. Inhibiting the function of the receptor in sensory neurons using selective drugs or genetically removing the gene significantly increases nerve fibre growth.
We propose a “cholinergic constraint hypothesis” describing a role for acetylcholine in restricting the growth of nerves within the skin.

The general objectives are:

  1. To suppress the muscarinic receptor pathway to repair nerve endings damaged by diabetes or anti-cancer agents.
  2. To determine the mechanism whereby receptor blockade enhances nerve growth with a focus on a role in the control of calcium signalling and mitochondrial function.

Impact statement

The proposed studies have strong translational potential if successful. Our work with topical delivery of muscarinic blocking drugs (already USFDA-approved for another indication) has progressed to a point where one small phase 2 clinical trial is complete and additional studies are envisaged to be completed by February 2022 for the treatment of diabetic neuropathy. The USFDA has awarded our novel topical formulation an IND with fast track designation. A company, WinSanTor, Inc., has been set up and will oversee the delivery of this plan. This proposal, if funded, will enable the work to broaden in scope and permit this therapeutic approach to be performed in a wide range of distal dying back neurodegenerative diseases.

Correcting aberrant axonal bioenergetics to drive nerve repair in neurological disease.

(Ben Gurion Univ/St. Boniface Foundation) Defects in neuronal energy supply occur in several neurological diseases, including Alzheimer’s disease and neuropathies of the peripheral nervous system (PNS). We recently showed that antimuscarinic drugs enhance mitochondrial function and drive nerve repair in a variety of neuropathic diseases of the PNS, including HIV neuropathy and diabetic neuropathy. These drugs work by blocking, through an unknown mechanism, an endogenous cholinergic pathway that is inhibitory to mitochondrial function and axonal outgrowth. Drugs with selective or specific antagonism of the muscarinic acetylcholine type 1 receptor (M1R) were most efficacious.


We will test if suppression of M1R signalling leads to enhanced Ca2+ signalling and activation of the Ca2+/calmodulin-dependent protein kinase kinase  (CaMKK and AMP-activated protein kinase (AMPK) pathway that augments mitochondrial function at multiple levels to drive axonal outgrowth and survival.


In vitro studies using adult sensory neurons will aim to identify Ca2+ channels, for example, TRPM3, required for raised Ca2+ subsequent to antimuscarinic treatment. Intracellular Ca2+ and mitochondrial function will be imaged simultaneously and in parallel-energy status will be determined using real-time imaging with ATP biosensors (ATeam constructs). Complementary studies will fully characterize mitochondrial function using the Seahorse XF24 analyzer. Previous work in diabetic humans and animals models reveals decreased sensory innervation of the cornea. Thus, non-invasive in vivo confocal imaging of the cornea will be used to study ATP levels in sensory nerve endings derived from the trigeminal ganglion of mice with neuronal-specific Thy1.2-driven ATeam expression. In vitro and in vivo studies with sensory neurons will be performed using normal and type 1 diabetic mice (mice will be made diabetic with streptozotocin) and the impact of the diabetic state on bioenergetics, e.g. [ATP], in live axons will be determined for the first time. Antimuscarinic drugs will be applied topically to the cornea to attempt to reverse bioenergetic deficits and stimulate nerve growth. For the in vitro work, control studies will be performed with sensory neurons derived from M1R knockout mice to prove the involvement of M1R.

Specific Aims

AIM 1 Mechanism of antimuscarinic drug-induced enhancement of mitochondrial function via Ca2+ mobilization in cultured adult neurons. 

AIM 2 Non-invasive confocal in vivo imaging to determine the mechanism of antimuscarinic drug action in sensory fibres of the cornea of diabetic mice.


These comprehensive studies will directly link for the first time sub-optimal energy production associated with diabetes, with impaired axonal regeneration in neuropathy, and will identify the mechanism of action of antimuscarinic drugs. Commercialization is underway with these drugs for the treatment of peripheral neuropathy. Phase 2 trials in persons with type 2 diabetes are planned. These proposed studies will elevate our understanding of the mechanism of drug action and, hopefully, will accelerate translation to the bedside.

Energy failure in nerve fibres: its detection and therapeutic reversal in neurological disease. (Bank of Montreal)

Background in neurological diseases of the central and peripheral nervous systems (CNS and PNS) studies reveal that impaired mitochondrial function leads to the neurodegeneration of nerve cells and their circuits (dendrites, axons and synapses) (Chowdhury, Smith et al. 2013, Cai and Tammineni 2016). Disease processes such as Alzheimer’s and diabetes directly impact mitochondrial physiology to cause a down-regulation in the ability of the organelle to supply energy (in the form of ATP). Failure of energy supply leads to impaired electrical excitability and sup-optimal ion homeostasis in nerve cells that triggers cell death and degeneration (Bennett, Doyle et al. 2014). The degeneration of synapses and nerve endings leads to loss of connectivity in the nervous system and drives impaired cognition and sensation (Cashman and Hoke 2015). At present, there are no therapies that can reverse these neurodegenerative processes.

Specific Aims

We recently published work in the Journal of Clinical Investigation showing that antimuscarinic drugs can be utilized to augment mitochondrial function and drive nerve repair (Calcutt, Smith et al. 2017). The main purpose of the current work is to reveal the mechanism of action of these drugs using an in vivo approach that is non-invasive. Mouse models of Alzheimer’s or peripheral neuropathy will be utilized and the ability of antimuscarinic drugs to reverse nerve damage will be determined while live imaging the same nerve fibres. New optical techniques permit real-time imaging of nerve fibres in the cornea (Tavakoli, Petropoulos et al. 2013). It is known in human disease and related animal models that the nerve fibres innervating the cornea undergo neurodegeneration (Chen, Frizzi et al. 2013, De Clerck, Schouten et al. 2015). Therefore, we hypothesize that during neurological disease the nerve fibres in the cornea will degenerate and this will be due to mitochondrial dysfunction driven by stressors related to diabetes or Alzheimer’s. There are the following specific aims:

  • Aim 1 (year 1) – Live imaging of the corneal nerve fibres to reveal degeneration of fibres in animal models of CNS and PNS disease.
  • Aim 2 (years 2-3) – In vivo quantification of abnormalities in mitochondrial function and energy supply in nerve fibres.
  • Aim 3 (years 4-5) – Use antimuscarinic drugs for therapy in animal models of Alzheimer’s and type 1 diabetes and determine if mitochondrial dysfunction and fibre loss can be reversed.

SPOR Network in diabetes and its related complications.


Individuals with diabetes, representing ~10% of Canadians, are deeply concerned about their risk of developing blindness, limb amputations, kidney and heart failure, and hypoglycemia. Among the most vulnerable, these complications are underdiagnosed and often ineffectively treated. Patients and non-research health professionals have joined our SPOR Network to redefine interventions for the earliest diagnosis and customized treatments that will transform healthcare for all individuals with diabetes. Building on programs of excellence, our team of experts in biomedical, clinical, population and health services research, education, and knowledge translation (KT) will bridge Valleys 1 and 2 (KT gaps 1 and 2) with the following projects.


Recognizing successful models of early detection, with primary and specialty (e.g., retinopathy) care networks in BC, AB, MB, ON, QC and NS (rural, urban-rural, urban) we will launch a complications screening pilot studies to identify the best evidence-based diagnostic and data collection methods. While documenting the prevalence and incidence of diabetes in these communities, we will establish the platform for a national registry to evaluate access to and implementation of effective methods for diagnosing complications: retinopathy, nephropathy, neuropathy and cardiovascular disease. We will capture health determinants relevant to risk and progression of complications (sex, gender, socio-economic status, ethnocultural background, geography, lifestyle [diet and physical activity]) and co-morbidities (e.g., arthritis) and link this information with electronic medical records and population administrative data. By applying advanced analytics on this converged data we will develop algorithms for complex complications risk assessment necessary for the design of a unique Canadian Risk Calculator.

This smartphone communications tool will be used by patients and their healthcare providers to facilitate shared decision-making and the implementation of customized care paths. By linking clinical information about complication trajectories with new knowledge about glucose-triggered biological factors (genetics, medical imaging of affected organs, physiological study of heart and kidney function), we will identify the biomarkers of high and low risk for complications. These biomarkers will guide our first-in-human trials of therapeutics targeted at specific diabetes complications for those at high risk.

Our national patient registry and trials management platforms will provide well-phenotyped subjects for large-scale clinical and genomics studies. To achieve the best glycemic control with minimal hypoglycemia, we will evaluate the applicability and efficacy of leading-edge insulin pump therapy and a novel standards-based external artificial pancreas using a smartphone app to monitor glucose control, physical activity and other modulators. In multicentered trials, we will test new therapies discovered by our scientists for diabetic heart and kidney disease, retinopathy and neuropathy. Complementary approaches evaluated in multicentered trials will include diet and lifestyle interventions, and disease target-specific new diagnostics and therapies. Expanding on successful trials (e.g., Vigorous Physical Activity for Glycemic Control) in diabetes we will focus on the needs of populations most vulnerable to poor health outcomes (e.g., First Nations communities). We will apply easy-to-implement web-based tools with user-centred design to assess lifestyle measures (physical activity and diet) and the efficacy of personalized behaviour-modifying interventions. Informed by our Researchers-Research User’s (patients and care providers) Partnership Platform our scientists and trainees will be trained in patient-oriented research with a focus on chronic disease. We will identify where evidence about effective intervention to prevent and treat diabetes complications can drive improved health policy and cost-effective system solutions.


Our national SPOR Network will change the trajectory of diabetes complications by establishing evidence-based models of best prevention and care paths uniquely customized for patients at greatest risk, a model applicable to all chronic disease management.

Drug discovery and commercialization

A Juvenile Diabetes Research Foundation (JDRF)/NIH-funded drug screen by the Fernyhough lab in 2007-2008 identified antimuscarinic drugs as potential drivers of nerve repair in adult sensory neurons. Drs. Paul Fernyhough and Nigel Calcutt (UCSD) collaborated on a JDRF team grant starting in 2008 to perform preclinical studies to fully characterize the utility of these drugs for the treatment of diabetic neuropathy. These two labs complement each other with Fernyhough focusing on in vitro and in vivo mechanistic work and the Calcutt lab providing expertise in a variety of mouse models of neuropathy and associated clinically relevant endpoints (e.g. quantification of intraepidermal nerve fibre density in footpad). Between 2010 and 2017 this work received several sources of grant support including JDRF, CIHR and NIH. These studies generated a Journal of Clinical Investigation publication in early 2017 showing that specific or selective antagonists of muscarinic acetylcholine type 1 receptors protected from nerve damage in diabetic neuropathy, chemotherapy-induced peripheral neuropathy and a model of HIV-induced neuropathy. A new paper in Frontiers in Neuroscience is now published, one paper is accepted subject to revision at Neuropharmacology and a third paper is about to be submitted to Neuropharmacology. The submission of this muscarinic receptor-related work has been delayed to safeguard commercialization activities.

Starting in late 2010, patents were initiated via the University of Manitoba. Currently, one patent has been granted in Canada, Europe and China. Drs. Calcutt, Fernyhough and a medicinal chemist from UHN, Dr. Lakshmi Kotra, set up a small biotech start-up called WinSanTor Inc ( in late 2011 (CEO Stanley Kim). This enterprise licensed this IP from these institutes in 2012 and has instigated drug development of antimuscarinic drugs for the treatment of peripheral neuropathies. The company has successfully obtained funding support from NIH, totalling nearly US$11million, via the SBIR/STTR programs. The primary aim has been to develop topical formulations of antimuscarinic drugs, particularly pirenzepine, for therapy in neuropathic diseases. This funding has been used to support toxicity studies, pharmacokinetic work, topical formulation development, drug manufacture and a now successfully completed phase 1 trial. A small phase 2 trial in type 2 diabetic patients has been completed and showed efficacy with a topical antimuscarinic with respect to the quality of life, neuropathic endpoints and IENF levels in the skin. Larger phase 2 trials in Canada, Denmark, Germany and the USA are planned with topical pirenzepine in diabetic patients for early 2019 onwards via funding derived from a SPOR chronic disease network grant ( and company resources.

At this stage the exact mechanism and/or site of action of these drugs in the context of nerve repair is unknown. It is also unknown how endogenous acetylcholine exactly modulates axonal plasticity in vivo. New studies are planned with Dr. Yves De Koninck (UofLaval) who brings unique in vivo electrophysiology and calcium imaging expertise of the DRG and distal axon to drive this work forward. While drug development continues our work aims to provide key basic science knowledge in regard to the role of endogenous acetylcholine in regulating nerve growth and identify the precise targets of antimuscarinic drug action.

Fernyhough Top 10 publications – January 2019

  1. *Sabbir, M.G. and P. Fernyhough (2018). Muscarinic receptor antagonists activate ERK-CREB signalling to augment neurite outgrowth of adult sensory neurons. Neuropharmacology. 143, 268-281.
  2. *Aghanoori, M.-R., Smith, D.R., Levari-Shariati, S., Ajisebutu, A., Nguyen, A., Desmond, F., Calcutt, N.A., Aliani, M. and Fernyhough(2018). Insulin-like growth factor-1 augments mitochondrial function through AMPK to drive axonal repair and protect from sensory neuropathy in type 1 diabetes. Molecular Metabolism. 20, 149-165.
  3. *Schartner, E., Sabbir, M.G., Saleh, A., Silva, R.V., Roy Chowdhury, S., Smith, D.R. and P. Fernyhough (2018). High glucose concentration suppresses a SIRT2 regulated pathway that enhances neurite outgrowth in cultured adult sensory neurons. Experimental Neurology. 309, 134-147.
  4. *Calcutt, N.A., Smith, D.R., Frizzi, K., Roy Chowdhury, S.K., Mixcoatl-Zecuatl, T., Saleh, A., Muttalib, N., Van der Ploeg, R., Ochoa, J., Sabbir, M.G., Gopaul, A., Tessler, L., Wess, J., Jolivalt, and P. Fernyhough (2017). Selective antagonism of muscarinic receptors is neuroprotective in peripheral neuropathy. Journal of Clinical Investigation. 127, 608-622. (if, 12.6).
  5. Dhingra, R., Margulets, V., Roy Chowdhury, S.K., Thliveris, J., Jassal, D., Fernyhough, P., Dorn, G., and L.A. Kirshenbaum (2014). Bnip3 mediates doxorubicin-induced cardiac myocytes necrosis and mortality through changes in mitochondrial signalling. Proceedings of the National Academy of Sciences, USA. 111, E5537-5544. (if, 9.8)
  6. *Roy Chowdhury, S.K., Smith, D.R.and P. Fernyhough (2013). The role of aberrant mitochondrial bioenergetics in diabetic neuropathy. Neurobiology of Disease. 51, 56-65. (if, 5.12)
  7. *Roy Chowdhury, S.K., Smith, D.R., Saleh, A., Schapansky, J., Marquez, A., Gomes, S., Akude, E., Morrow, D., Calcutt, N.A. and P. Fernyhough (2012). Impaired AMP-activated protein kinase signalling in dorsal root ganglia neurons is linked to mitochondrial dysfunction and peripheral neuropathy in diabetes. Brain. 135, 1751-1766. (if, 9.23)
  8. *Akude, E., Zherebitskaya, E., Roy Chowdhury,, Smith, D.R., Dobrowsky, R.T. and P. Fernyhough (2011). Diminished superoxide generation is associated with respiratory chain dysfunction and changes in the mitochondrial proteome of sensory neurons from diabetic rats. Diabetes. 60, 287-299. (if, 8.9)
  9. *Roy Chowdhury, S. K., Zherebitskaya, E., Smith, D.R., Akude, E., Chattopadhyay, S., Jolivalt, C.G., Calcutt, N.A. and P. Fernyhough (2010). Mitochondrial respiratory chain dysfunction in lumbar dorsal root ganglia of streptozotocin-induced diabetic rats and its correction by insulin treatment.59, 1082-1091. (if, 8.9)
  10. *Zherebitskaya, E., Akude, E., Smith, D.R. and P. Fernyhough (2009). Development of selective axonopathy in adult sensory neurons isolated from diabetic rats: role of glucose-induced oxidative stress. . Diabetes. 58, 1356-1364. (if, 8.5)



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2014 Senator Duhamel Award for Research Innovation

2008 Juvenile Diabetes Research Foundation, Mary Jane Kugel Award

2007 University of Manitoba Presidential Outreach Award

2006 Juvenile Diabetes Research Foundation, Mary Jane Kugel Award

1993 – 1998 Wellcome Trust Postdoctoral Fellowship Pharmacology $ 700,000
Department of Pharmacology
Queen Mary & Westfield College
University of London, United Kingdom

1991 – 1993 Merck, Sharp & Dome Pharmacology $100,000
Postdoctoral Fellowship Research Award
St. Bartholomew’s Medical College
Queen Mary & Westfield College
University of London, United Kingdom

1987 – 1989 MRC Postdoctoral Fellowship Award Cell Biology $ 90,000
MRC Cell Biophysics Unit, King’s College
London, United Kingdom

1981 – 1984 BBSRC Ph.D. Scholarship Research Award Biochemistry $ 30,000
University of Sheffield, United Kingdom

Listing of active grants

2019 – 2024
Canadian Institutes of Health Research
Total $1,090,125. (with $100k matching from WinSanTor)
Operating grant: Muscarinic receptor antagonism as a novel mechanism for sensory nerve repair.
PI: Fernyhough, P.; Co-PIs: DeKoninck, Y., U of Laval & Calcutt, N.A., UCSD

St Boniface | Ben Gurion Univ. Partnership
Total $300,000.
Correcting aberrant axonal bioenergetics to drive nerve repair in neurological disease.
PI: Fernyhough, P.; Co-PI: Gitler, D.

Bank of Montreal Award
Total $250,000.
Energy failure in nerve fibres: its detection and therapeutic reversal in neurological disease.
PI: Fernyhough, P.

Mitacs Accelerate International
Total:  $180,000
Development of specific peptide antagonists of muscarinic receptors to repair the nervous system
PI:  Fernyhough,, P.

2019 – 2024
Canadian Institutes of Health Research 
Total $1,090,125.
Operating grant: Muscarinic receptor antagonism as a novel mechanism for sensory nerve repair.
PI: Fernyhough, P.; Co-PIs: DeKoninck, Y., U of Laval & Calcutt, N.A., UCSD

2019 – 2020
St. Boniface Foundation
Total:  $100,000
Drug studies on the peripheral nervous system.
PI:  Fernyhough, P.

St Boniface | Ben Gurion Univ. Partnership
Total $300,000.
Correcting aberrant axonal bioenergetics to drive nerve repair in neurological disease.  
PI: Fernyhough, P.; Co-PI: Gitler, D.

Bank of Montreal Award             
Total $250,000.
Energy failure in nerve fibres: its detection and therapeutic reversal in neurological disease.
PI: Fernyhough, P.

WinSanTor Biosciences Inc.

In Fall 2017 we obtained US$298,550 through the NIH STTR program to fund studies in CIPN.
Title: Development of pirenzepine for CIPN.
NIH Grant #:  1R41CA213555-01A1  PI: Andrew Mizisin, WinSanTor Biosciences Inc

In Spring 2017 the company was funded via NIH Commercialization Readiness Program (CRP). Funding for one year of US$997,000.
Title: Assessment of chronic toxicity to support the use of topical pirenzepine for treating diabetic neuropathy. NIH Grant #: 2SB1DK104512-04 PI: Stanley Kim, CEO WinSanTor Biosciences Inc

In Fall 2014 we obtained US$2.25million through NIH SBIR (Fast Track; via NIDDK) program to fund further drug development. Rated highest application in competition.
Title: Pre-Clinical Development of Topical Pirenzepine for Treating Diabetic Neuropathy.
NIH Grant #: 1R44DK104512-01 PI: Stanley KIM, CEO WinSanTor Biosciences Inc

In Fall 2012 we obtained US$7.3million through the NIH Type 1 Diabetes – Rapid Access to Intervention Development (T1D-RAID; via NIDDK) program that will oversee the development of the drug.
Title: Topical pirenzepine to treat diabetic neuropathy.
PI: Stanley KIM, CEO WinSanTor Biosciences Inc


Current Research group

Darrell Smith – Senior Scientist

Farhana Naznin – Post Doctoral Fellow

TM Zaved Waise – Post Doctoral Fellow

Shayan Amiri –  Ph.D. Graduate Student

Sanjana Chauhan – Ph.D. Graduate Student

Pranav Mishra Ph.D. Graduate Student

Doris Goubran –  Undergraduate Student

Amila Hoang – Undergraduate student

Annie Jiang – Undergraduate Student

Marvellous Oyeyode – Undergraduate Student

Serena Phillips –  Undergraduate Student

Lauren Verhaeghe – Undergraduate Student

Jeffrey Wilson – Undergraduate Student 

Lori Tessler –  Technician

Debbie Fowler – Glasswash Technician

Kelly Jorundson – Administrative Manager