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Victor Rusu

Principal at Apple Tree Partners

Greater Boston

Overview 

Victor Rusu is currently a Principal at Apple Tree Partners, specializing in genome editing, cell biology, and molecular biology. With a PhD from Harvard University and experience at institutions like Citi and Jnana Therapeutics, he has a strong background in bioinformatics and NGS data analysis, making significant contributions to the biotech sector.

Work Experience 

  • Principal

    2019 - Current

Apple Tree Partners is a venture capital firm that invests in pharmaceuticals, biotech, medtech, and healthcare services.

Raised $5,000,000.00.

  • Senior Biotechnology Associate at Citi

    2018 - 2019

    • Wrote initiation reports. Created company specific models and performed DCF valuation. • Regularly wrote notes on stock moving events and updates on quarterly earnings. Maintained company specific models. • Assisted with the design, execution, and analysis of physician surveys.

Citigroup is a financial services holding company that provides various financial products and services.

Raised $12,950,000,000.00 from ValueAct Capital and Abu Dhabi Investment Authority.

  • Senior Scientist

    2017 - 2018

    • Founding scientist. Involved from the beginning. Helped establish the lab. Contributed to setting company priorities and defining scientific strategy including target selection. • Lead biologist on lead project. Developed cell-based assays for small molecule screening.

Jnana Therapeutics develops innovative therapies using a chemoproteomics drug discovery platform.

Raised $207,000,000.00 from AbbVie, Avalon Ventures, Bain Capital Life Sciences, RA Capital Management, Polaris Partners, Pfizer Venture Investments and Versant Ventures.

  • PhD Graduate Student

    2012 - 2017

    • Research led to first-author Cell paper converging on a novel therapeutic mechanism for type 2 diabetes (T2D). • Identified the causal variants and the causal gene at a previously uncharacterized genetic locus which harbors some of the largest common genetic risk factors for T2D. Determined distinct molecular mechanisms through which (coding and noncoding) mutations in the previously uncharacterized gene, SLC16A11, increase T2D risk. • Characterized function of SLC16A11 and impact of T2D risk mutations using unbiased methods: next generation sequencing, metabolomics, and proteomics. Analyzed datasets and wrote custom scripts as needed. This work led to the identification and functional characterization of a key PPI which is disrupted and underlies the mechanism through which coding mutations in SLC16A11 lead to a T2D-associated metabolic profile (as demonstrated by loss-of-function experiments in primary human hepatocytes). • Discovered an eQTL at the locus. Demonstrated that T2D risk noncoding mutations disrupt SLC16A11 gene regulation through allele specific ddPCR and ChIP-seq in primary human hepatocytes and patient samples. • Generated CRISPR/Cas9 Slc16a11 knockout mouse models and characterized mice.

Articles About Victor

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