Gopal Ramakrishnan Email & Phone Number

Developing Next-Generation Potentially Curative Immunotherapies for Late-Stage Liquid and Solid Cancers and Autoimmune DiseasesWe are a clinical-stage cell therapy and immuno-oncology company located in the Greater San Diego Area specializing in the development of Next-Generation Potentially Curative Immunotherapies for Late-Stage Liquid and Solid Cancers. Our groundbreaking therapeutic solution addresses critical unmet medical challenges in cancer medicine, especially, with regard to enabling curative hematopoietic stem-cell transplantation to become safer and more efficacious with TZ101 and developing our next-generation Tumor Infiltrating Lympocyte (TIL) therapies i.e FucoTILs with the goal to transform survival for late-stage cancer patients with solid cancer tumors. We are laser-focused on the development of our breakthrough proprietary cell therapies that use specialized immune cells from the patient or the donor to target/eliminate cancer cells regulate and treat inflammation and life-threatening side effects from standard-of-care cancer therapies. Powered by our innovative proprietary cell efficacy multiplier technology, our cancer immunotherapy drugs aim to simultaneously enable precise immune cell delivery to the disease sites as well as amplification of the innate power of the patient’s immune cells to effectively eradicate, cure and even prevent cancer. Targazyme is an early pioneer of cellular therapy and has accumulated the experience of advancing a portfolio of innovative products, achieving regulatory milestones including a Phase 3 Special Protocol Assessment (SPA) award from the FDA, and obtaining multiple FDA orphan-drug designations and a BLA pathway that enables 12 years of protection from generic drugs.

Carlsbad, California, United States

We are a clinical-stage cell therapy and immuno-oncology company located in the Greater San Diego area specializing in the development of Next-Generation Potentially Curative Immunotherapies for Late-Stage Liquid and Solid Cancers and Autoimmune Diseases

Chicago, Illinois, United States

The lab works on the intersection of cell signalling and metabolism in the realm of oncology and immuno-oncology. We are exploring the roles of Hexokinases, AKT and AMPK in the above phenomena. We found that HK2 is selectively upregulated during cancer formation and one of the mechanisms by which it regulates tumour growth and metastasis is through stabilizing the expression of PD-L1 and SNAIL. Our work on AKT showed that AKT1 specifically regulates metastasis by affecting neutrophil recruitment to the primary tumour. We also found that AMPK can function as a pro-tumorigenic and pro-metastatic factor by neutralizing ROS production via selectively promoting unsaturated fatty acid metabolism through CD36.Areas of work: Oncology, Immuno-Oncology, Cancer Metabolism, Molecular Biology, BiomarkersSkills acquired: Preclinical Models, 3D Cell Culture, Organoid Culture, NGS, scRNA, Exome and Deep Sequencing, Metabolic Labelling and GC-MS, PDX/Immunodeficient Models, Primary Cell Culture, MATLAB, Dataset Analysis

Jackson, Mississippi, United States

1. Explored the role of NF1 (Neurofibromin1) mutations in the development of lung cancer and pancreatic cancer, where it emerged as a significant driving mutation in those tumours that lack an alteration in the KRas locus. The second project was on the role of the TGIF-YAP1 signalling axis in the development of Lung Adenocarcinoma.2. The research included the identification of novel transcriptional targets of mutant p53 that may mediate its ability to extend proliferative lifespan, abrogate the normal response to oncogenic signals and to promote chemotherapy resistance. This involved leveraging the basic understandings of mutant p53 transcriptional regulatory to identify liabilities that are clinically relevant.3. Work on AKT, AMPK and 14-3-3 signalling, with the identification of new AKT interacting modulators and substrates. We identified Notch4 to be regulated by AKT phosphorylation at four distinct sites that resulted in the cytoplasmic retention by binding to 14-3-3 and abrogated its transcriptional activity. We were also able to map the detailed binding between AKT/14-3-3 and FoxO3. We found Sirt1 and Sirt2 deacetylases to be critical binding partners in regulating AKT activation and showed that Sirt2 undergoes phosphorylation by AMP kinase at T101 causing it to bind to AKT. A separate project dealt with the expression of the modulation of NAD levels on lifespan and longevity. We generated transgenic mice expressing the Drosophila nicotinamidase (dNAAM) gene in all tissues and showed that these mice were resistant to calorie induced weight gain and stress induced cell death. Areas of work: Oncology, Cell Signalling, Post-transcriptional Modifications, Proteomics, Molecular Biology, Transcriptional Regulation, BiomarkersSkills acquired: Transgenic and GEMM Models, ChIP/ChIP-Seq, LC-MS, Isotopic Labelling and 2D Phosphopeptide Mapping, Transgenic Mice Generation, Antibody Generation, Mini Bioreactor Cell Culture

Doctor Of Philosophy - Phd, Biochemistry

Master'S Degree, Molecular And Human Genetics