Dr. Baker is the Clinical Chief in the Division of Immunology and Rheumatology at Stanford University. He received his bachelor's degree from Pomona College, his medical degree from Harvard Medical School, and his master's degree in Epidemiology and Clinical Research from Stanford University. He completed his Internal Medicine residency at the Massachusetts General Hospital and his Rheumatology fellowship at Stanford University. Dr. Baker has established a clinical research program that is focused on clinical trials and bench-to-bedside translational research. He has designed and led investigator-initiated studies with a focus on sarcoidosis, Sjogren’s syndrome, and IgG4-related disease. In addition, he is a founder and Co-Director of the Stanford Multidisciplinary Sarcoidosis Program and collaborates with other team members to advance sarcoidosis clinical care and research.
- IgG4-related disease
- Sjogren's syndrome
- Cardiac sarcoidosis
- Systemic lupus erythematosus
- Rheumatoid Arthritis
Clinical Assistant Professor, Medicine - Immunology & Rheumatology
Clinical Chief, Division of Immunology and Rheumatology, Department of Medicine, Stanford University (2020 - Present)
Honors & Awards
Translational Research and Applied Medicine Award, Stanford University (9/1/18 - 9/1/19)
Scientist Development Award, Rheumatology Research Foundation (2/1/17 - 1/31/18)
KL2 Stanford Spectrum Mentored Career Development Award, National Institutes of Health (7/1/17 - 6/30/19)
Distinguished Fellow Award, American College of Rheumatology (11/28/16)
Bevra Hahn Distinguished Fellow Scholarship, California Rheumatology Alliance (5/24/16)
Ruth L. Kirschstein National Research Service Award, National Institutes of Health (7/1/16 - 1/31/17)
ACR/EULAR Exchange Program Award, American College of Rheumatology (6/12/17)
Master of Science, Stanford University, EPIDM-MS (2019)
Board Certification: Internal Medicine, American Board of Internal Medicine (2014)
Fellowship: Stanford University Rheumatology Fellowship (2016) CA
Board Certification: Rheumatology, American Board of Internal Medicine (2016)
Residency: Massachusetts General Hospital Internal Medicine Residency (2014) MA
Medical Education: Harvard Medical School (2011) MA
Bachelor of Arts, Pomona College (2004)
Efficacy and Safety of GSK3196165 (Otilimab) Versus Placebo and Sarilumab in Participants With Moderately to Severely Active Rheumatoid Arthritis Who Have an Inadequate Response to Biological Disease-modifying Antirheumatic Drug (DMARDs) and/or Janus Kinase (JAK) Inhibitors
This study (contRAst 3 [202018: NCT04134728]) is a Phase 3, randomized, multicenter, double-blind study to assess the safety and efficacy of GSK3196165 in combination with conventional (cs) DMARD[s]) or the treatment of adult participants with moderate to severe active rheumatoid arthritis (RA) who have had an inadequate response to biologic (b) DMARD[s]) and/or JAK inhibitors. The study will consist of a screening phase of up to 6 weeks followed by 24 week treatment phase in which participants will be randomized in ratio of 6:6:6:1:1:1 to GSK3196165 150 milligrams (mg) subcutaneously (SC) weekly,GSK3196165 90 mg SC weekly, sarilumab 200 mg SC every other week or placebo (three arms) respectively, all in combination with background csDMARD(s). At Week 12, participants in the three placebo arms will switch from placebo to active intervention (either GSK3196165 150 mg SC weekly, GSK3196165 90 mg SC weekly, or sarilumab 200 mg SC every other week). Participants who, in investigator's judgement will benefit from extended treatment with GSK3196165, may be included in the long-term extension study (contRAst X [209564: NCT04333147]). Any participant who does not transition into study 209564 will undergo a safety follow-up visit at Week 34 (corresponding to 12 weeks after the last potential dose of sarilumab, at Week 22).
Long-term Safety and Efficacy of GSK3196165 (Otilimab) in the Treatment of Rheumatoid Arthritis (RA)
RA is a chronic, systemic inflammatory autoimmune disease which requires treatment for a long time period, hence it is important to study the long-term safety and efficacy of the continuous treatment with GSK3196165 over several years. This is a Phase 3, multicenter, parallel group treatment and long-term extension study primarily to assess safety with efficacy assessment as a secondary objective. Adult participants with RA who have completed the treatment phase of a qualifying GSK3196165 clinical studies (Phase 3 studies contRAst 1 (201790: NCT03980483), contRAst 2 (201791: NCT03970837) and contRAst 3 (202018: NCT04134728) and who, in investigator's judgement will benefit from extended treatment with GSK3196165 will be included in this study (contRAst X [209564: NCT04333147]). Participants will continue to receive the same background conventional synthetic disease modifying anti-rheumatic drug(s) [csDMARD(s)] treatment as they received in their qualifying study. Eligible participants will be enrolled to receive weekly GSK3196165 90 milligrams (mg) or 150 mg by subcutaneous (SC) injection. The anticipated study duration is approximately 4 years which will enable participants to receive treatment with GSK3196165 until it is expected to become commercially available. Approximately 3000 participants from the qualifying studies will participate in this long-term extension study.
Sarilumab in Patients With Glucocorticoid-Dependent Sarcoidosis
The purpose of this study is to compare the effectiveness and the safety of sarilumab in patients with glucocorticoid-dependent sarcoidosis.
A Crossover Study to Compare RAYOS to IR Prednisone to Improve Fatigue and Morning Symptoms for SLE
To compare the effect of RAYOS® versus immediate-release (IR) prednisone on fatigue as measured by Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-F).
Stanford is currently not accepting patients for this trial. For more information, please contact Mark Genovese, 650-498-5630.
A Study Comparing Upadacitinib (ABT-494) to Placebo in Participants With Active Psoriatic Arthritis Who Have a History of Inadequate Response to at Least One Biologic Disease Modifying Anti-Rheumatic Drug
This is a Phase 3 multicenter study that includes two periods. Period 1 is designed to compare the safety, tolerability, and efficacy of ABT-494 Dose A once daily (QD) and Dose B QD versus placebo in participants with moderately to severely active Psoriatic Arthritis (PsA) who have an inadequate response to Biological Disease Modifying Anti-Rheumatic Drug (bDMARDs). Period 2 evaluates the safety, tolerability and efficacy of ABT-494 Dose A QD and Dose B QD in subjects with PsA who have completed Period 1.
Stanford is currently not accepting patients for this trial.
Study to Evaluate the Safety and Efficacy of Filgotinib and Lanraplenib in Adults With Lupus Membranous Nephropathy (LMN)
The primary objective of this study is to evaluate the efficacy of filgotinib and lanraplenib (previously GS-9876) in adults with lupus membranous nephropathy (LMN).
Stanford is currently not accepting patients for this trial.
Osteoarthritis risk is reduced after treatment with ticagrelor compared to clopidogrel: a propensity score matching analysis.
Arthritis & rheumatology (Hoboken, N.J.)
Osteoarthritis (OA) is a common cause of joint pain and disability, and effective treatments are lacking. Extracellular adenosine has anti-inflammatory effects and can prevent and treat OA in animal models. Ticagrelor and clopidogrel are both used in patients with coronary artery disease, but only ticagrelor increases extracellular adenosine. The aim of this study was to determine whether treatment with ticagrelor was associated with a lower risk of OA.We conducted a 1:2 propensity score matching analysis using the Optum Clinformatics™ Data Mart from 2011 to 2017. We included patients who received either ticagrelor or clopidogrel for at least 90 days and excluded those with a prior diagnosis of OA or inflammatory arthritis. OA was identified using International Classification of Diseases codes. The primary outcome was the time to diagnosis of OA after treatment with ticagrelor versus clopidogrel.Our propensity score matched cohort consisted of 7,007 ticagrelor-treated patients and 14,014 clopidogrel-treated patients, with a median number of days on treatment of 287 and 284 respectively. For both groups, the mean age was 64 years, and 73% of the patients were male. Multivariate Cox-regression analysis estimated a hazard ratio of 0.71 (95% CI 0.64-0.79, p<0.001) for developing OA after treatment with ticagrelor compared to clopidogrel.Treatment with ticagrelor was associated with a 29% lower risk of developing OA compared to clopidogrel over five years of follow-up. We hypothesize that the reduction in OA seen in patients who received ticagrelor may in part be due to increased extracellular adenosine.
View details for DOI 10.1002/art.41412
View details for PubMedID 32564514
Novel Approach to the Treatment of Cardiac Sarcoidosis with TNF-alpha Inhibition
View details for Web of Science ID 000507466900378
- Dermatomyositis Associated With a Skull Base Chondrosarcoma JCR-JOURNAL OF CLINICAL RHEUMATOLOGY 2019; 25 (4): E50–E53
TNF-alpha inhibition for the treatment of cardiac sarcoidosis.
Seminars in arthritis and rheumatism
Tumor necrosis factor alpha (TNF-α) inhibitors are increasingly being used for treating refractory cardiac sarcoidosis. There is a theoretical risk, however, that these therapies can worsen heart failure, and reports on efficacy and safety are lacking.We conducted a retrospective review of all cardiac sarcoidosis patients seen at Stanford University from 2009 to 2018. Data were collected on patient demographics, diagnostic testing, and treatment outcomes.We identified 77 cardiac sarcoidosis patients, of which 20 (26%) received TNF-α inhibitor treatment. The majority were treated for progressive heart failure or tachyarrhythmia, along with worsening imaging findings. All TNF-α inhibitor treated patients demonstrated meaningful benefit, as assessed by changes in advanced imaging, echocardiographic measures of cardiac function, and prednisone use.A large cohort (n = 77) of cardiac sarcoidosis patients has been treated at Stanford University. Roughly one-fourth of these patients (n = 20) received TNF-α inhibitors. Of these patients, none had worsening heart failure and all saw clinical benefit. These results help support the use of TNF-α inhibitors for the treatment of cardiac sarcoidosis based on real-world evidence and highlight the need for future prospective studies.
View details for DOI 10.1016/j.semarthrit.2019.11.004
View details for PubMedID 31806154
Security and Privacy Qualities of Medical Devices: An Analysis of FDA Postmarket Surveillance
2012; 7 (7)
Medical devices increasingly depend on computing functions such as wireless communication and Internet connectivity for software-based control of therapies and network-based transmission of patients' stored medical information. These computing capabilities introduce security and privacy risks, yet little is known about the prevalence of such risks within the clinical setting.We used three comprehensive, publicly available databases maintained by the Food and Drug Administration (FDA) to evaluate recalls and adverse events related to security and privacy risks of medical devices.Review of weekly enforcement reports identified 1,845 recalls; 605 (32.8%) of these included computers, 35 (1.9%) stored patient data, and 31 (1.7%) were capable of wireless communication. Searches of databases specific to recalls and adverse events identified only one event with a specific connection to security or privacy. Software-related recalls were relatively common, and most (81.8%) mentioned the possibility of upgrades, though only half of these provided specific instructions for the update mechanism.Our review of recalls and adverse events from federal government databases reveals sharp inconsistencies with databases at individual providers with respect to security and privacy risks. Recalls related to software may increase security risks because of unprotected update and correction mechanisms. To detect signals of security and privacy problems that adversely affect public health, federal postmarket surveillance strategies should rethink how to effectively and efficiently collect data on security and privacy problems in devices that increasingly depend on computing systems susceptible to malware.
View details for DOI 10.1371/journal.pone.0040200
View details for Web of Science ID 000306956300012
View details for PubMedID 22829874
View details for PubMedCentralID PMC3400651
Enhancement of DNA tumor vaccine efficacy by gene gun-mediated codelivery of threshold amounts of plasmid-encoded helper antigen
2009; 113 (1): 37-45
Nucleic acid-based vaccines are effective in infectious disease models but have yielded disappointing results in tumor models when tumor-associated self-antigens are used. Incorporation of helper epitopes from foreign antigens into tumor vaccines might enhance the immunogenicity of DNA vaccines without increasing toxicity. However, generation of fusion constructs encoding both tumor and helper antigens may be difficult, and resulting proteins have unpredictable physical and immunologic properties. Furthermore, simultaneous production of equal amounts of highly immunogenic helper and weakly immunogenic tumor antigens in situ could favor development of responses against the helper antigen rather than the antigen of interest. We assessed the ability of 2 helper antigens (beta-galactosidase or fragment C of tetanus toxin) encoded by one plasmid to augment responses to a self-antigen (lymphoma-associated T-cell receptor) encoded by a separate plasmid after codelivery into skin by gene gun. This approach allowed adjustment of the relative ratios of helper and tumor antigen plasmids to optimize helper effects. Incorporation of threshold (minimally immunogenic) amounts of helper antigen plasmid into a DNA vaccine regimen dramatically increased T cell-dependent protective immunity initiated by plasmid-encoded tumor-associated T-cell receptor antigen. This simple strategy can easily be incorporated into future vaccine trials in experimental animals and possibly in humans.
View details for DOI 10.1182/blood-2008-01-136267
View details for Web of Science ID 000262162800010
View details for PubMedID 18832136
View details for PubMedCentralID PMC2614641