Bio

I am an MD from Chung Shan Medical University, Taiwan. Before coming to Stanford, I obtained my MS degree in epidemiology at Harvard T.H. Chan School of Public Health, Boston, MA, where I completed graduate training in clinical, pharmacologic, and genetic epidemiology, and pursued advanced skills in biostatistics and causal inference.

My past research focused on real-world epidemiology studies using patient registries and national health insurance databases to elucidate the predictors or risk factors of immunologic diseases. For my graduate study, I conducted pharmacoepidemiology studies using electronic health record (EHR) data to elucidate the predictors of anti-drug antibodies development and its correlation to autoimmunity, to identify the generation of immunogenicity that may impact the effectiveness of monoclonal antibody therapies in individuals with autoimmune diseases. I gained experience in genetic data manipulation to investigate polymorphisms in response to monoclonal antibody therapies in asthma patients.

At Stanford, I am involved in research on the identification of molecular determinants of cardiometabolic diseases.

Professional Education

  • Master of Science, Harvard T.H. Chan School of Public Health, Boston, MA, Epidemiology (2023)
  • Doctor of Medicine, Chung Shan Medical University, Taichung, Taiwan, Medicine (2021)

Stanford Advisors

Contact

  • Academic
    mlichen@stanford.edu
    University - Scholar Department: School of Medicine Position: Postdoctoral Scholar

Additional Info

Links

All Publications

  • Incidence of Anti-Drug Antibodies to Monoclonal Antibodies in Asthma: A Systematic Review and Meta-Analysis JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY-IN PRACTICE Chen, M., Nopsopon, T., Akenroye, A. 2023; 11 (5): 1475-+

    Abstract

    Antidrug antibodies (ADAs) may worsen the efficacy and safety of biologics. However, little is known about the incidence of ADAs associated with the 6 biologics approved for the treatment of asthma in the United States.To elucidate the incidence of ADAs and their impact on reported clinical outcomes.Systematic review and meta-analyses of randomized controlled trials, open-label extension studies, and nonrandomized studies of biologics in patients with asthma indexed in PubMed, Embase, and CENTRAL between January 1, 2000, and July 9, 2022, were carried out. The primary outcomes were treatment-emergent ADAs (incidence) and ADA prevalence.A total of 46 studies met the eligibility criteria. ADA incidence over follow-up was 2.91% (95% CI, 1.60-4.55) and was highest in the benralizumab studies (8.35%), with a risk ratio of 4.9 (2.69-8.92) when compared with placebo, and lowest in the omalizumab studies (0.00%). Incidence was 7.61% in the dupilumab studies, 4.39% in reslizumab, 3.63% in mepolizumab, and 1.12% in the tezepelumab studies. Incidence of neutralizing antibodies was 0.00% to 10.74% and was highest for benralizumab (7.12%). Incidence of neutralizing antibodies was higher in the benralizumab every 8 weeks (8.17%) versus every 4 weeks arms (5.81%). Results were consistent in subgroup analyses by study type and length of follow-up.Approximately 2.9% of individuals in the included studies developed ADAs over study follow-up period. The incidence was highest in the benralizumab group and lowest in the omalizumab group. The subcutaneous route and longer dosing intervals were associated with higher ADA development.

    View details for DOI 10.1016/j.jaip.2022.12.046

    View details for Web of Science ID 001025725300001

    View details for PubMedID 36716995

  • Comparative efficacy of tezepelumab to mepolizumab, benralizumab, and dupilumab in eosinophilic asthma: A Bayesian network meta-analysis JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY Nopsopon, T., Lassiter, G., Chen, M., Alexander, C., Keet, C., Hong, H., Akenroye, A. 2023; 151 (3): 747-755

    Abstract

    It is unclear how the efficacy of tezepelumab, approved for the treatment of type 2 high and low asthma, compares to the efficacy of other biologics for type 2-high asthma.We sought to conduct an indirect comparison of tezepelumab to dupilumab, benralizumab, and mepolizumab in the treatment of eosinophilic asthma.The investigators conducted a systematic review and Bayesian network meta-analyses. They identified randomized controlled trials indexed in PubMed, Embase, or Cochrane Central Register of Controlled Trials (CENTRAL) between January 1, 2000, and August 12, 2022. Outcomes included exacerbation rates, prebronchodilator FEV1, and the Asthma Control Questionnaire.Ten randomized controlled trials (n = 9201) met eligibility. Tezepelumab (relative risk: 0.63; 95% credible interval [CI]: 0.46-0.86) was associated with significantly lower exacerbation rates than benralizumab and larger improvements in FEV1 compared to mepolizumab (mean difference [MD]: 66; 95% CI: -33 to 170) and benralizumab (MD: 62; 95% CI: -22 to 150), though the 95% CI crossed the null value of 0. Mepolizumab improved the Asthma Control Questionnaire score the most, but this improvement was not significantly different from that of tezepelumab (tezepelumab vs mepolizumab; MD: 0.14; 95% CI: -0.10 to 0.38). For efficacy by clinically important thresholds, tezepelumab, mepolizumab, and dupilumab achieved a >99% probability of reducing exacerbation rates by ≥50% compared to placebo, but benralizumab had only a 66% probability of doing so. Tezepelumab and dupilumab had a probability of 1.00 of improving prebronchodilator FEV1 by ≥100 mL above placebo. Compared to mepolizumab, dupilumab had >90% chance for improving FEV1 by ≥50 mL, but none of the differences between biologics exceeded 100 mL.In individuals with eosinophilic asthma, tezepelumab and dupilumab were associated with greater improvements (although below clinical thresholds) in exacerbation rates and lung function than benralizumab or mepolizumab.

    View details for DOI 10.1016/j.jaci.2022.11.021

    View details for Web of Science ID 001025005600001

    View details for PubMedID 36538979

    View details for PubMedCentralID PMC9992307

https://orcid.org/0000-0003-0276-2626