Alfred L. Garfall
· Associate Professor of Medicine (Hematology-Oncology) at the Hospital of the University of PennsylvaniaVerifiedUniversity of Pennsylvania · Rehabilitation Medicine
Active 2007–2026
About
Alfred L. Garfall, MD, MS, is an Associate Professor of Medicine (Hematology-Oncology) at the Hospital of the University of Pennsylvania and the Multiple Myeloma Section Chief in the Division of Hematology/Oncology at the Department of Medicine, Perelman School of Medicine, University of Pennsylvania. His clinical expertise includes multiple myeloma, plasma cell disorders, and bone marrow transplantation. Dr. Garfall is also the Director of Autologous Hematopoietic Cell Transplantation, Cell Therapy, and Transplant Program at the Hospital of the University of Pennsylvania. His educational background includes an AB in Molecular Biology from Princeton University, an MD from New York University School of Medicine, and an MS in Translational Research from the University of Pennsylvania. His research focuses on clinical trials, immunotherapy, and translational research related to hematologic malignancies, particularly multiple myeloma. Dr. Garfall has contributed to the development of CAR T cell therapies targeting CD19 and BCMA for multiple myeloma, and his work includes investigating the response and toxicity of anti-CD19 CAR T cell therapy, as well as the use of bispecific antibodies such as Teclistamab. His research aims to improve treatment outcomes for patients with multiple myeloma through innovative immunotherapeutic approaches.
Research signals
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Research topics
- Medicine
- Internal medicine
- Immunology
- Oncology
- Cancer research
- Family medicine
- Biology
- Pharmacology
Selected publications
Cancer · 2026-01-01
articleOpen accessBACKGROUND: Teclistamab is the first approved bispecific antibody targeting B-cell maturation antigen. It has demonstrated rapid, deep, durable responses with manageable safety in patients with triple-class exposed relapsed/refractory multiple myeloma (TCE RRMM). METHODS: The authors report results from three cohorts: Global Trial cohort consisting of 217 patients from three registrational studies (pivotal MajesTEC-1 study [n = 165], China cohort of MajesTEC-1 [n = 26], and the Japan MMY1002 study [n = 26]); the subset of 52 of 217 patients formed the Asian Trial cohort, and 42 patients treated outside of trials in the pre-approval access (PAA) program formed the Asian PAA cohort. RESULTS: In the Global Trial cohort, median age was 65 years, weight was 69 kg, and prior lines-of-therapy was five; 29.0% had high-risk cytogenetics and 18.9% had extramedullary disease. With 29.5 months median follow-up, overall response rate (ORR)/≥complete response (CR) was 66.4%/50.2%, median duration of response (DOR) was not reached; progression-free survival (PFS) and overall survival (OS) were 15.6, and 29.1 months, respectively. In the subset of Asian Trial cohort, baseline features were similar except for lower weight (median, 58 kg); median follow-up was 26.3 months. ORR/≥CR was 76.9%/63.5%, 24-month DOR, PFS, and OS rates were 67.5%, 59.5%, 71.4%, respectively, with medians not yet reached. Efficacy was consistent in the Asian PAA cohort with ORR/≥CR of 66.7%/40.5%. Most common adverse events were cytopenias, cytokine release syndrome, and infections. Infection management improved over time, supported by increased immunoglobulin use in later-enrolling Asian studies, aligned with guideline adoption. CONCLUSION: Teclistamab demonstrated clinically meaningful benefits across diverse patients, encompassing various weight categories and geographies, reinforcing its potential as a standard of care for TCE RRMM. TRIAL REGISTRATION: ClinicalTrials.gov MajesTEC-1 (NCT03145181 and NCT04557098) and Japan MMY1002 study (NCT04696809).
Nature Biomedical Engineering · 2026-03-09 · 4 citations
articleTargeted Oncology · 2026-03-26
articleOpen accessTeclistamab is a B cell maturation antigen × CD3 bispecific antibody approved for relapsed/refractory multiple myeloma. Two step-up doses (SUDs) are used to mitigate the risk of cytokine release syndrome (CRS). For patients who experience dose delays, it is uncertain what length of delay necessitates repeat SUDs. We used modeling simulations and retrospective analysis of the phase 1/2 MajesTEC-1 study to optimize recommendations for repeat SUDs after teclistamab dose delay. Population pharmacokinetic modeling was used to simulate teclistamab serum concentrations after dose delays to assess the duration required to achieve levels comparable to estimated trough concentrations (Ctrough) following SUDs. Quantitative systems pharmacology modeling was used to simulate cytokine dynamics. Modeling-informed time windows were applied to a retrospective analysis of CRS data from MajesTEC-1 recommended phase 2 dose cohorts to further evaluate CRS incidence with prolonged dose delays (> 28 days). Median teclistamab serum concentrations were estimated to drop to levels comparable to the simulated SUD 2 median Ctrough after 62 days and SUD 1 median Ctrough after 111 days. Simulated cytokine peaks at treatment restart during weekly or biweekly dosing at these intervals were lower than those following the initial SUD. Retrospective analysis of clinical data revealed a low incidence of CRS (grade 1–2; 2/61 [3.3%]) upon resuming teclistamab as recommended following a dose delay. These analyses suggest teclistamab can be safely restarted without repeat SUD for delays ≤ 62 days, and at SUD 2 for delays 63–111 days. For delays > 111 days, both SUDs should be administered as instructed per label before resuming treatment at 1.5 mg/kg. NCT03145181 (phase 1, May 9, 2017); NCT04557098 (phase 2, September 21, 2020). Teclistamab is used to treat patients with multiple myeloma, a type of blood cancer, that has returned after prior treatment (relapsed) or that does not respond to other treatments (refractory). Patients treated with teclistamab first receive two lower doses (step-up doses) to reduce the risk of side effects, including cytokine release syndrome. Cytokine release syndrome is caused by the rapid release of immune-signaling proteins called cytokines into the bloodstream and can result in fever, low blood pressure, and low blood oxygen levels. After step-up dosing, patients are dosed with 1.5 mg/kg once weekly. Patients who achieve a complete response or better and maintain it for at least 6 months can switch to 1.5 mg/kg every other week dosing. Some patients may need to delay teclistamab dosing to help manage side effects or due to other circumstances. We used mathematical model-based simulations to estimate how dose delays would affect serum levels of teclistamab and cytokines; these models suggested that, following dose delays, teclistamab serum levels would be comparable to, and cytokine levels lower than, the levels estimated after step-up doses. Importantly, data from the MajesTEC-1 clinical trial showed that only two of the 61 patients with dosing delays of more than 28 days experienced cytokine release syndrome; all events were low severity. Overall, modeling results and clinical trial data supported an update of the recommendations for restarting teclistamab.
Rab5 improves CAR T cell efficacy via reducing fratricide and maintaining surface CAR levels
The Journal of Experimental Medicine · 2026-03-27 · 1 citations
articleWe show continuous tumor exposure results in a loss of chimeric antigen receptor (CAR) T cell (CART) endocytic activity due to downregulation of Rab5. Loss of endocytic activity exacerbates the effects of trogocytosis, the bidirectional transfer of tumor target antigens and CARs between malignant cells and CARTs, resulting in CART dysfunction and fratricide. Constitutive expression of Rab5 within the CARTs reduced fratricide by reducing the amount of trogocytosed antigens on the cell surface, while simultaneously enhancing CAR availability through dissociation of CAR from target, recycling unbound CAR back to the plasma membrane, and limiting CAR capture by tumor cells. Rab5-expressing CARTs exhibited superior antitumor activity in both BCMA-CARTs isolated from the bone marrow of treated patients and mesothelin-specific CARTs in a solid tumor model. These studies uncover an unexpected relationship between endocytosis and CART function and suggest that pairing Rab5 with CAR expression could improve the clinical efficacy of CART therapy.
Nature Medicine · 2026-01-15 · 2 citations
articleOpen access2025-11-11
articleOpen access<p>Supplemental Table S8: Multivariable regression for overall response</p>
2025-11-03
articleOpen access<p>Supplemental Table 2: Prior BCMA-directed therapy details</p>
2025-11-11
articleOpen access<p>Supplemental Table 7: Univariable regression for overall response</p>
2025-11-11
articleOpen access<p>Supplemental Table 2: Prior BCMA-directed therapy details</p>
2025-11-24
articleOpen access1st authorCorresponding<p>Supplemental tables: (1) Subject characteristics. (2) Cytogenetic profiles and high-risk features. (3) Prior treatment exposures and refractoriness. (4) CAR T cell product characteristics. (5) Products that did not meet target dose. (6) Adverse events of grade 3-4. (7) Cytokine release syndrome and ICANS. (8). Maintenance therapy. Supplemental Figures: (1) Study schematic and subject disposition, (2) Correlates of manufacturing success, (3) Hematopoietic recovery, (4) Post-infusion T cell phenotypes, (5) Correlates of in vivo expansion and manufacturing success, (6) Late post-infusion CAR T cell re-expansion, (7) Soluble BCMA, (8) Late-onset clinical responses, (9) MM cell BCMA expression, (10) Pre- and post-treatment Sox2-specific T cell responses in CART-BCMA monotherapy patients, (11) Pre- and post-treatment Sox2-specific T cell responses in CART-BCMA + huCART19 combination therapy patients, (12) Sustained post-treatment SOX2-specific T-cell responses.</p>
Frequent coauthors
- 115 shared
Edward A. Stadtmauer
University of Pennsylvania
- 96 shared
Adam D. Cohen
University of Pennsylvania
- 93 shared
Dan T. Vogl
Hospital of the University of Pennsylvania
- 58 shared
Jakub Svoboda
University of Pennsylvania
- 55 shared
Niels W.C.J. van de Donk
- 55 shared
Carl H. June
Parker Institute for Cancer Immunotherapy
- 54 shared
Elise A. Chong
Hospital of the University of Pennsylvania
- 54 shared
Adam Waxman
University of Pennsylvania
Education
- 2002
B.A., Molecular Biology
Princeton University
- 2008
M.D.
New York University School of Medicine
- 2014
M.S., Translational Research
University of Pennsylvania
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