International Conference on Pharmaceutical Oncology July 18-19, 2018 Atlanta, Georgia, USA

Biography:

Rudolf Lucas obtained his PhD in cellular and genetic biotechnology in 1993 summa cum laude from the Free University of Brussels, Belgium (VUB) and he currently holds a faculty position at the Medical College of Georgia. He is currently Chair of the American Heart Association Lung Fellowship Committee. His expertise mainly

lies in the development of novel therapeutic candidates to treat pulmonary edema. Over the past 20 years, his research has led to the discovery of a TNF-derived peptide, Solnatide, which is a direct activator of the epithelial sodium channel. This peptide has shown promising activities in two recently finalized phase 2a clinical trials in patients with acute lung injury and upon lung transplantation.

Abstract:

Efficient exchange of oxygen and carbon dioxide between the lung capillaries and the alveoli requires that the latter is kept dry. Vectorial Na+ transport through the apically expressed epithelial sodium channel (ENaC), and the basolaterally expressed Na+-K+-ATPase mediates Alveolar liquid Clearance (ALC) in type 1/2 alveolar epithelial cells. ENaC activity is defined by the product of its open probability time and its membrane surface expression. The alpha subunit of ENaC also associates with the acid-sensing ion channel to form the hybrid Non-Selective Cation (NSC) Channel, which also contributes to ALC. In conditions of ARDS and severe pneumonia, which are associated with intense pulmonary inflammation, ENaC function can become impaired. Moreover, pathogen-associated toxins, as well as pro-inflammatory cytokines can disrupt capillary endothelial barriers, causing fluid to leak from the capillaries into the alveolar space. The resulting Pulmonary Permeability Edema (PPE)

is a potentially lethal complication, for which no proven pharmacological treatment exists to date. The identification of novel

therapeutics for PPE is therefore of the utmost importance. Solnatide is a TNF-derived peptide that mimics the lectin-like domain of tumor necrosis factor, the latter of which is spatially distinct from the receptor binding sites1-4. Solnatide binds to the alpha subunit of ENaC and as such increases the open probability, as well as surface expression of the channel, even in the presence of bacterial toxins, such as Pneumolysin (PLY), the main virulence factor of Streptococcus pneumoniae. The peptide also prevents bacterial toxin-induced endothelial barrier dysfunction in lung microvascular endothelial cells, which express both ENaC and NSC channels and has potent anti-inflammatory actions. The therapeutic potential of Solnatide was recently evaluated in two phase clinical trials in patients with acute lung injury and lung transplantation. The results of the pre-clinical and clinical studies will be discussed in this contribution.

Biography:

SH Ansari obtained his BPharm in 1979 from University of Delhi, MPharm in 1981 from Punjab University, Chandigarh and PhD in Pharmacognosy and Phytochemistry in 1997 from Jamia Hamdard. He was conferred Doctor of Science in 2002 by International University of Contemporary Studies, Washington, USA. Professor Ansari, having teaching and research experience of more than 36 years, has served Jamia Hamdard, in different capacities as Head, Department of Pharmacognosy and Phytochemistry, Dean School of Pharmaceutical Education and Research, Dean Students’ Welfare, and Director, School of Open and Distance learning and as Vice Chancellor as well. Presently working as Professor in Department of Pharmacognosy and Phytochemistry in School of Pharmaceutical Education and Research. He has been bestowed with “Best Young Pharmacy Teacher Award 1997-98”, “Life Time Achievement Award” by United Writers’ Association, Chennai, Pharma Ratan Award for Life Time Achievement by Rab Di Meher Society, 2016. “Gold Medal of Excellence” by the Open University of Complimentary Medicines, Colombo, Sri Lanka in 1998. Professor Ansari also has 215 research papers to his credit.

Abstract:

The global acceptability of herbal drugs and traditional medicines are still challenged due to its complex nature and quality control analysis. Due to this the stability analysis of herbal drugs, botanicals, and traditional medicine is very complicated and needs proper attention in this field. However uses of bioactive markers for the analysis stability of these drugs are in common practice, which gives an insight and at least an answer to the complexity in analysis. Use of biologically active molecules for analysis of stability, shelf life and pharmacokinetics is very useful for understanding biology and mechanism of action of these traditionally used drugs as well as makes it easy. Triphala is a very common drug used in traditional ayurvedic and unani medicines for the treatment of various diseases and very frequently used in Indian system of medicine. It is composed of powder fruits of Emblica officinalis, Termenalia chebula and Termenalia bellerica in a uniform ratio. The phenolic antioxidants like Gallic Acid, Tannic Acid (Termenalia chebula, Termenalia bellerica) and Quercetin (Emblica officinalis) are common biomarkers present in these fruits. Hence in present investigation the stability of Triphala was established using Gallic acid, Tannic acid and Quercetin by expressing the samples at different temperatures and humidity as per the WHO guidelines at bench top and at accelerated stability conditions. The results of the study showed that constant of these markers as much affected in stored conditions.

Biography:

Hiroshi Kobayashi received his PhD in Biochemistry from University of Tokyo in 1974. After his postdoctoral training at Colorado University Medical Center, he started to study adaptation strategies of microorganisms to acidic environments at Chiba University in 1978. His research is focused on mammalian cell functions under acidic conditions from 1996 at Graduate School of Pharmaceutical Sciences, Chiba University. His current research interest is cancer chemotherapy with drugs specific to acidic nests. He retired in 2012 and is now a professor emeritus at Chiba University. He works as an associate editor of International Immunopharmacology published by Elsevier from 2014.

Abstract:

It is well known that cancer nests are often acidified. The acidity may affect anti-cancer chemotherapy and immune responses.

Our group found that the cytosolic pH decreased in cancer cells proliferating in acidic medium and approximately 700 genes were expressed at a higher level in such cells, leading us to suppose that an anti-cancer drug whose target is the product of such genes may work in acidic cancer nests with less of effects on alkaline normal tissues. We established the in vitro assay system for screening anti-cancer drugs working in acidic nests, and approximately 300 compounds were examined using various cancer cell lines. Among them, four compounds, Lovastatin, Cantharidin, Manumycin A, and Ionomycin, were found to have anti-cancer activity preferentially at acidic pH. Next, the anti-cancer activity of statins was focused. Promising results of statins as an anti-cancer drug have been reported in mouse models and cancer patients. Stains have been used in patients with hyperlipidemia and side effects have been reported in less than 1% patients, supporting that anti-cancer drugs working preferentially in acidic cancer nests have less of effects on normal tissues whose pH is slightly alkaline. Since alkaline medium has been used for screening of drugs, it would be highly possible that novel anti-cancer drugs with fewer side effects would be exploited using our methods. Our experimental system would be also useful for elucidation of immune functions in acidic cancer nests. It was shown with this method that TCR signaling does not work under acidic conditions.

Biography:

After her MD from Medical school of University Kunming, China and her PHD thesis on inner ear cell degeneration and therapies from University of Montpellier, France. Jing Wang is the team leader of “Sensory loss and rescue” group at the Institute of Neurosciences of Montpellier, Montpellier, France. During her career, Jing Wang published 36 papers in international journals (web of science h-Index: 19, citations, 1040 citations), 9 book chapters and more than 150 communications or posters. She is member of the Editorial Boards of international journals. In addition to basic research, she took out 3 patents for tinnitus and deafness treatments and promoted translational research.

Abstract:

In recent years, with the improvement of cancer survival through more effective treatment, the emphasis has been in trying to minimize the side effects caused by chemo and radiotherapy, to ensure that patients have the best quality of life throughout their cancer journey. The tumour suppressor p53 is widely implicated in a broad range of cancers. Indeed, p53 is either mutated or inactivated in the majority of cancers. Abundant evidence indicates that toxicity caused by DNA-damaging anticancer therapies in normal tissues is also mainly mediated by p53. p53 accumulates in the cells shortly after anticancer challenges and acts as a nuclear transcription factor that modulates the expression of numerous p53-responsive genes (e.g. p21Waf1, 14- 3-3-σ, Mdm2, cyclin G, Bax). This initiates a cascade of events leading to massive programmed cell death in specific normal tissues during the systemic genotoxic stress associated with chemo and radiotherapies. This makes p53 a target for therapeutic suppression: An approach to reduce side effects associated with treatment of p53-deficient cancers. Here I summarize the role of p53 and the possibilities of its manipulation to improve side effects during active treatment through survivorship.

Biography:

Arkesh Mehta is a lifelong entrepreneur with experience up and down the biopharmaceutical spectrum since his first startup more than 15 years ago. Arkesh has co-founded and/or served as CEO or Executive Chairman for a set of leading-edge biotechnology, molecular diagnostics and healthcare IT companies. All of these companies had successful exits including BPI technologies, AT-GC BioPharm, Avanti NanoSciences and CBTEK. Arkesh is an advisor and Board member of several bio and healthcare startups. He has organized, Chaired or participated in number of international panels, including organizing the First NASDAQ panel on Bio-IT. He is a member of Trustees for Sushita Group, a non-profit that fosters entrepreneurship.

Abstract:

To keep up with the pace of change required to deliver a compelling precision therapeutic product and to leverage emerging technologies, we propose a three-tier architecture that provides numerous benefits. It allows a drug developer the opportunity to extend, modularize, and be able to configure their lead compound in a clinical candidate. The architecture shortens time to market and reduces the cost to integrate new clinical functionalities into clinical-outcome focused, patient-centric precision therapeutic.  It can also maximize patient adoption through the flexibility it provides when integrating patient-friendly properties into existing drug formulations and therapeutic applications. “3-tier precision therapeutic architecture is a therapeutic drug-clinical functionality architecture in which the functional process logic, drug release, targeting function and clinical function interface are developed and maintained as independent modules”. A “tier” in this case can also be referred to as a “layer”. The three tiers, or layers, involved include: (a) A presentation layer that sends drug molecules to target sites in the form to elicit optimal efficiency. This might leverage clinical functions like targeting, protection from host defense, and ondemand controlled release, etc. (b) A clinical functional layer that uses an fictional fabric layer and processes the business logic for the seamless integration of clinical functionalities. (c) A drug core which is at the heart of the precision therapeurtic. This could be a single drug, acombination drug, immunooncology drugs or CRISPR/Cas system. Here we present outline of NanoBindi-a precision therapeutic development platform that meets all these objectives to turn lead candidates to clinical candidates.

Biography:

Arkesh Mehta is a lifelong entrepreneur with experience up and down the biopharmaceutical spectrum since his first startup more than 15 years ago. Arkesh has co-founded and/or served as CEO or Executive Chairman for a set of leading-edge biotechnology, molecular diagnostics and healthcare IT companies. All of these companies had successful exits including BPI technologies, AT-GC BioPharm, Avanti NanoSciences and CBTEK. Arkesh is an advisor and Board member of several bio and healthcare startups. He has organized, Chaired or participated in number of international panels, including organizing the First NASDAQ panel on Bio-IT. He is a member of Trustees for Sushita Group, a non-profit that fosters entrepreneurship.

Abstract:

To keep up with the pace of change required to deliver a compelling precision therapeutic product and to leverage emerging technologies, we propose a three-tier architecture that provides numerous benefits. It allows a drug developer the opportunity to extend, modularize, and be able to configure their lead compound in a clinical candidate. The architecture shortens time to market and reduces the cost to integrate new clinical functionalities into clinical-outcome focused, patient-centric precision therapeutic.  It can also maximize patient adoption through the flexibility it provides when integrating patient-friendly properties into existing drug formulations and therapeutic applications. “3-tier precision therapeutic architecture is a therapeutic drug-clinical functionality architecture in which the functional process logic, drug release, targeting function and clinical function interface are developed and maintained as independent modules”. A “tier” in this case can also be referred to as a “layer”. The three tiers, or layers, involved include: (a) A presentation layer that sends drug molecules to target sites in the form to elicit optimal efficiency. This might leverage clinical functions like targeting, protection from host defense, and ondemand controlled release, etc. (b) A clinical functional layer that uses an fictional fabric layer and processes the business logic for the seamless integration of clinical functionalities. (c) A drug core which is at the heart of the precision therapeurtic. This could be a single drug, acombination drug, immunooncology drugs or CRISPR/Cas system. Here we present outline of NanoBindi-a precision therapeutic development platform that meets all these objectives to turn lead candidates to clinical candidates.