Exhibit 99.1

Poseida Therapeutics Presents New Phase 1 Data at AACR 2024 Supporting Potential of P-BCMA-ALLO1 Allogeneic CAR-T Therapy to Benefit Broad Range of Patients with Multiple Myeloma

– Promising early data suggest patients with relapsed/refractory multiple myeloma who progressed after prior BCMA-targeted therapy achieved clinical responses with P-BCMA-ALLO1, which was well tolerated

– Following efforts to optimize allogeneic CAR-T therapy, Poseida is presenting a new data analysis underscoring the need for higher lymphodepletion chemotherapy doses when treating solid tumors vs. multiple myeloma

SAN DIEGO, April 8, 2024 – Poseida Therapeutics, Inc. (Nasdaq: PSTX), a clinical-stage cell and gene therapy company advancing a new class of treatments for patients with cancer and rare diseases, today announced new data from a subset of patients in an ongoing Phase 1 study of its lead program, P-BCMA-ALLO1. Results showed that three of the five (60%) patients with relapsed/refractory multiple myeloma who had progressed following BCMA-targeted therapy achieved clinical responses with P-BCMA-ALLO1. In addition, this investigational treatment was well-tolerated.

P-BCMA-ALLO1 is a novel investigational B-cell maturation antigen (BCMA)-targeted allogeneic, T stem cell memory (T_SCM)-rich chimeric antigen receptor T-cell (CAR-T) therapy manufactured from healthy donor T-cells and available off-the-shelf. These new Phase 1 study subgroup data and a new data analysis of different lymphodepletion regimens in patients treated with P-BCMA-ALLO1 for multiple myeloma or P-MUC1C-ALLO1 for solid tumors are being presented today in a poster session at the American Association for Cancer Research (AACR) Annual Meeting 2024 in San Diego.

“Multiple myeloma remains incurable, and patients often relapse, despite initial high response rates with BCMA-targeted immunotherapies, including autologous CAR-T therapies,” said Bhagirathbhai Dholaria, M.D., Associate Professor of Medicine (Hematology/Oncology) at the Vanderbilt-Ingram Cancer Center in Nashville, Tenn. “New treatment options are urgently needed for these patients, which is why I’m encouraged by these impressive Phase 1 subgroup results, which may be the first report of an allogeneic CAR-T therapy showing clinical activity in heavily pretreated patients whose myeloma has progressed after multiple BCMA-targeted immunotherapies.”

“These new data build on the P-BCMA-ALLO1 data presented at ASH 2023, which demonstrated a 100% overall response rate in patients who had not been previously treated with a BCMA-targeted therapy. The new findings also provide additional evidence that our investigational, off-the-shelf allogeneic CAR-T therapy could be an appropriate treatment for a broader range of patients with multiple myeloma, including those with relapsed/refractory disease whose cancer progressed following prior BCMA-targeted therapy, representing the highest unmet need in this setting,” said Syed Rizvi, M.D., Chief Medical Officer at Poseida. “In addition, we continue to explore the optimal lymphodepletion regimen for CAR-T in solid tumors and are directly applying these learnings to our P-MUC1C-ALLO1 trial with the goal of delivering the same benefits in solid tumors as we have seen in myeloma. We look forward to sharing more fulsome datasets on both our BCMA and MUC1-C programs in the second half of 2024.”

New Phase 1 P-BCMA-ALLO1 Study Subgroup Data

The open-label, multicenter Phase 1 dose-escalation study in patients with relapsed/refractory multiple myeloma is assessing the safety and maximum tolerated dose of P-BCMA-ALLO1 (primary objective) and its anti-myeloma activity (secondary objective). Study participants were required to have received a prior proteasome inhibitor, immunomodulatory drug and anti-CD38 monoclonal antibody. Five study participants who had progressed on or following prior BCMA-targeting autologous CAR-T, T-cell engagers or both, and with ninety days post-P-BCMA-ALLO1 treatment follow-up, are presented in this poster.

Key findings from the subgroup analysis showed that P-BCMA-ALLO1 was well tolerated with no dose-limiting toxicities, graft vs. host disease, or Grade 3 or greater cytokine release syndrome (CRS) or immune effector cell neurotoxicity syndrome (ICANS). The overall response rate in patients receiving P-BCMA-ALLO1 was 60%, with all three patients who achieved a clinical response experiencing a very good partial response (VGPR). This included one patient who had previously received both teclistamab and an autologous CAR-T therapy and has maintained a response for more than four months.

New Data on Optimizing Lymphodepletion (LD) Regimen for Patients with Solid Tumors Treated with Investigational Allogeneic CAR-T Therapy

As patients with multiple myeloma receive more bone marrow suppressive treatments than those with solid tumors during their treatment journeys, this analysis evaluated the effect of increasing amounts of cyclophosphamide in LD regimens to optimize CAR-T pharmacokinetics.

The analysis compared various LD regimens in two early Phase 1 trials of Poseida’s investigational allogeneic CAR-T cell therapies in patients with multiple myeloma and solid tumors. Results showed that patients with solid tumors may require higher cyclophosphamide doses to achieve adequate LD, which would provide a sufficient niche to support allogeneic CAR-T expansion.

Poster Presentation Details

About P-BCMA-ALLO1

P-BCMA-ALLO1 is an investigational allogeneic CAR-T therapy licensed to Roche that targets B-cell maturation antigen (BCMA) and is in Phase 1 clinical development for the treatment of patients with relapsed/refractory multiple myeloma. This allogeneic program includes a VH-based binder that targets BCMA. Phase 1 clinical data presented at ASH 2023 supports the Company’s belief that T_SCM-rich allogeneic CAR-Ts have the potential to offer effective, safe and reliable treatment addressing unmet needs in multiple myeloma. The U.S. Food and Drug Administration granted Orphan Drug Designation to P-BCMA-ALLO1 for the treatment of multiple myeloma. Additional information about the Phase 1 study is available at www.clinicaltrials.gov (NCT04960579).

About P-MUC1C-ALLO1

P-MUC1C-ALLO1 is an investigational allogeneic CAR-T therapy in Phase 1 clinical development for multiple solid tumor indications. Poseida believes P-MUC1C-ALLO1 has the potential to treat a wide range of solid tumors derived from epithelial cells, such as breast, ovarian, colorectal, lung, pancreatic and renal cancers, as well as other cancers expressing a cancer-specific form of the Mucin 1 protein (MUC1-C). P-MUC1C-ALLO1 is designed to be fully allogeneic, with genetic edits to eliminate or reduce both host-vs-graft and graft-vs-host alloreactivity. Poseida has demonstrated the elimination of tumor cells to undetectable levels in preclinical models of both breast and ovarian cancer. Additional information about the Phase 1 study is available at www.clinicaltrials.gov (NCT05239143).

About Poseida Therapeutics, Inc.

Poseida Therapeutics is a clinical-stage biopharmaceutical company advancing differentiated cell and gene therapies with the capacity to cure certain cancers and rare diseases. The Company’s pipeline includes allogeneic CAR-T cell therapy product candidates for both solid and liquid tumors as well as in vivo gene therapy product candidates that address patient populations with high unmet medical need. The Company’s approach to cell and gene therapies is based on its proprietary genetic editing platforms, including its non-viral piggyBac^® DNA Delivery System, Cas-CLOVER^™ Site-Specific Gene Editing System, Booster Molecule, and nanoparticle and hybrid gene delivery technologies as well as in-house GMP cell therapy manufacturing. The Company has formed a global strategic collaboration with Roche to unlock the promise of cell therapies for patients with hematological malignancies. Learn more at www.poseida.com and connect with Poseida on X and LinkedIn.

Forward-Looking Statements

Statements contained in this press release regarding matters that are not historical facts are “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995. Such forward-looking statements include statements regarding, among other things, expected plans with respect to clinical trials, including timing of regulatory submissions and approvals and clinical data updates; anticipated timelines and milestones with respect to the Company’s development programs and manufacturing activities and capabilities; the potential capabilities and benefits of the Company’s technology platforms and product candidates, including the efficacy, safety and reliability profile of such product candidates; the quotes from Drs. Dholaria and Rizvi; and the Company’s plans and strategy with respect to developing its technologies and product candidates. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements. These forward-looking statements are based upon the Company’s current expectations and involve assumptions that may never materialize or may prove to be incorrect. Actual results could differ materially from those anticipated in such forward-looking statements as a result of various risks and uncertainties, which include, without limitation, the Company’s reliance on third parties for various aspects of its business; risks and uncertainties associated with development and regulatory approval of novel product candidates in the biopharmaceutical industry; the Company’s ability to retain key scientific or management personnel; the fact that interim data from the Company’s clinical trials may change as more patient data become available and remain subject to audit and verification procedures that could result in material differences from the final data; the fact that subgroup data may differ from future results of the same study once additional data has been received; and the other risks described in the Company’s filings with the Securities and Exchange Commission. All forward-looking statements contained in this press release speak only as of the date on which they were made. The Company undertakes no obligation to update such statements to reflect events that occur or circumstances that exist after the date on which they were made, except as required by law.

# # #

Poseida Investor and Media Relations:

Alex Chapman

Senior Vice President, IR & Corporate Communications

IR@poseida.com

Sarah Thailing

Senior Director, IR & Corporate Communications

PR@poseida.com

Exhibit 99.2 CT071 Clinical Activity of P-BCMA-ALLO1, a B-cell Maturation Antigen (BCMA) Targeted Allogeneic Chimeric Antigen Receptor T-cell (CAR-T) Therapy, in Relapsed Refractory Multiple Myeloma (RRMM) Patients Following Progression on Prior BCMA Targeting Therapy Bhagirathbhai Dholaria1, Leyla Shune2, Andrew Kin3, Katherine McArthur4, Jeff D. Eskew4, Christopher E. Martin4, Sabrina Haag4, Joanne McCaigue4, Hamid Namini4, Samuel DePrimo4, Stacey Cranert4, Julia Coronella4, Devon Shedlock4, Rajesh Belani4 1Vanderbilt University Medical Center, Nashville, TN; 2Division of Hematological Malignancies and Cellular Therapeutics, University of Kansas Medical Center, Westwood, KS; 3Karmanos Cancer Institute, Wayne State University, Detroit, MI; 4Poseida Therapeutics, San Diego, CA BACKGROUND Study P-BCMA-ALLO1-001: open-label, multicenter, phase 1 study to Patient cellular kinetics (CK) and cytokine profiles assess the safety of P-BCMA-ALLO1 in patients with RRMM Patient 1 Patient 2 Patient 3 Despite therapeutic advances, multiple myeloma remains incurable. B-cell Maturation Antigen (BCMA) is a well validated myeloma antigen for 512 106 512 106 512 106—P—P—P ) ) ) which multiple targeted therapies are now approved. BCMA targeting immunotherapies, such as bispecific T-cell engagers (TCE) and autologous e n BC BC BC li 105 M line 105 M line 105 M CAR-T provide high response rates, but relapses are common. Autologous CAR-T are logistically challenging due to the need for apheresis, e 128 128 128 s A—se—A se A—prolonged manufacturing times and occasional manufacturing failures. Many patients suffer disease progression and require bridging therapy P-BCMA-ALLO1 Ba 4 Ba 4 Ba 4 infusion on day 0 Key Inclusion Criteria: 10 10 10 while awaiting autologous CAR-T manufacturing. Some patients die from disease progression while waiting for autologous CAR-T to be Follow up, potential for redosing rom 32 ALLO1 rom 32 ALLO1 rom 32 ALLO1 • RRMM as defined by the IMWG f 3 f 3 f 3 manufactured. TCE are hampered by the need for chronic dosing that is logistically challenging. Emerging data also indicate that autologous 10 (C 10 (C 10 (C FC FC ( ( FC Conditioning • Must have received PI, IMiDs & CD38 ( CAR-T have lower clinical activity in patients who have progressed on TCE. Lastly, patients who have progressed after a prior BCMA targeting SCREENING FOLLOW UP s s Chemotherapy s e 8 102 opie 8 102 opie 8 102 opie immunotherapy are an emerging area of high unmet need for whom there are few commercially available therapies. mAb or triple refractory n s / ine / s ine s / ki m g ok g m ok m g Long-term o 101 101 101 P-BCMA-ALLO1 is an allogeneic CAR-T therapy manufactured from healthy donor T-cells, that is available “ ff-the- h lf”, and is being evaluated Cyclophosphamide (300, 500, or 1,000 mg/m2) • ECOG 0 or 1 D t y D t y D 2 2 2 in a phase 1 clinical trial (P-BCMA-ALLO1-001; NCT04960579) in RRMM patients. This primary objective is to determine the maximum tolerated 2 follow-up Cyt NA) C NA) C NA) and Fludarabine (30 mg/m ) on days -5, -4, -3 100 100 100 dose of P-BCMA-ALLO1, and the key secondary objective is to investigate the anti-myeloma activity. The patients must have progressed on a 0 5 10 15 20 25 30 0 5 10 15 20 25 30 0 5 10 15 20 25 30 prior proteasome inhibitor, immunomodulatory drug and anti-CD38 monoclonal antibody. The study allows enrollment of patients who have Study Day Study Day Study Day received prior BCMA targeting therapy. The study is exploring escalating P-BCMA-ALLO1 doses and several different lymphodepletion PRIMARY OBJECTIVE Presented are patients that have received and • Assess safety and MTD based on DLT progressed on BCMA targeted therapies Patient 4 Patient 5 chemotherapy (LD) regimens. Here we report the safety and early efficacy results for the 5 patients who were treated with P-BCMA-ALLO1 after 512 106 512 106—P—P IL-8 2 ) B ) B Figure 1 – Serum levels of CK by having progressed on BCMA targeting CAR-T, TCE or both. These patients were treated in arms P1 (LD: cyclophosphamide (cy) 500 mg/m + P-BCMA-ALLO1 dose and LD arms evaluated, and no. of ne ne IL-6 SECONDARY OBJECTIVES 105 105 fludarabine (flu) 30 mg/m2 × 3 days) or arm P2 (LD: cy 1000 mg/m2 + flu 30 mg/m2 × 3 days) at a P-BCMA-ALLO1 dose of > 2 × 106 to <6 × 106 patients* infused at each cohort: eli CM eli IL-10 CM qPCR and cytokines are shown for s 128 A s 128 A—IFNg—patients 1 – 5 across study days. cells/kg. • Evaluate the anti-myeloma effect of P-BCMA-ALLO1 a A a A Arm P1 (Cy 500); N = 2 B 4 B P-BCMA-ALLO1 4 DL2† 10 10 Cytokines are shown normalized as Here we demonstrate that P-BCMA-ALLO1 has clinical activity in the post BCMA immunotherapy setting including in patients who have received • Study effect of cell dose & LD regimen selection to Arm P2 (Cy 1,000); N = 3 rom 32 LLO1 rom 32 LLO1 fold change from baseline. Missing f 3 f 3 multiple prior BCMA targeting immunotherapies. * † 6 6 10 ( 10 ( guide dose selection for pivotal studies minimum of 4 weeks follow-up; DL2 = 2 x 10 – 6 x 10 cells/kg C F Co C F Co data points for CK are due to ( pi( pi insufficient DNA yield. LOD of qPCR s 8 102 s 8 102 e e e e n s/ m n m s/ is 100 cp/µg. CK = cellular kinetics; g g Proprietary, non-viral approach to produce TSCM-rich, fully allogeneic Patient characteristics 101 101 cp/mg = transposon copies/mg of Cytoki 2 DN Cytoki 2 DN DNA. 0 A) 0 A) P-BCMA-ALLO1 CAR-T from healthy donors 10 10 Patient 0 5 10 15 20 25 30 0 5 10 15 20 25 30 Characteristics Study Day Study Day 1 2 3 4 5 Responding patients showed higher max IL-15 and IL-7 and lower day 4 62-year-old white 64-year-old white 45-year-old African 73-year-old white Demographics 57-year-old white Male female female American male female CD3+ lymphocytes Year Dx / # prior A B regimens 2015; 5 priors 2014; 5 priors 2015; 8 priors 2019; 8 priors 2013; 8 priors Figure 2 – A) Serum levels of LD associated cytokines IL-15 and Myeloma Diagnosis IgG; Kappa free light IgG; Lambda free light IgA; Kappa free light IgG; Kappa free IgG; Kappa free light IL-7 and chemokine MCP-1 (Day Subtype chain chain chain light chain chain 0) are shown for patients 1 – 5 across study days. IL-15 and IL-7 Target or Measurable Extramedullary disease Absent Absent Absent Absent shown as max values over D0 – Plasmacytoma present D14. B) Absolute lymphocytes (total), CD4 or CD8 at Day 4. High-risk MM Cytogenetics Standard risk Standard risk Standard risk Standard risk Non-responding patients (1 & 4) (t(14:20)) are highlighted in RED. Prior anti-BCMA P-BCMA-101 (AUTO), Belantamab, JCARH125, CAR-T and anti- Teclistamab Abecma Belantamab Teclistamab Teclistamab BCMA therapy BCMA MESF 4341; 40% NR 2432; 37% 2703; 19% 6705; 26% Preliminary clinical activity in heavily pre-treated and BCMA % + previously BCMA exposed patients P-BCMA-ALLO1 2 S 2 VG R 2 VG R 1 S 1 VG R Response (BOR) * P-BCMA-ALLO1 CRS Gr 2 (D10-12) Febrile neutropenia Related None CRS Gr 1(D5 -8) CRS Gr 2 (D14-16) ICANS G1/2 (D14-17) (D13-15) Figure 3 – Duration of response for SAEs patients dosed with P-BCMA-ALLO1 *BOR includes confirmed and unconfirmed responses. Data cutoff: March 18th, 2024 at DL2 with LD containing 500 2 2 mg/m (P1) or 1000 mg/m (P2) cyclophosphamide. Events shown Heavily pretreated patients with prior PD on BCMA targeted agents include both confirmed and unconfirmed responses. Arrow indicates patients still in follow up. †Day -49 * *G5 AE aspiration pneumonia (assessed as unrelated) at day +45 † Day -796 †Data cut date: March 18th, 2024 CONCLUSIONS †Day -75 • P-BCMA-ALLO1 is a TSCM-rich allogeneic CAR-T manufactured from healthy donor cells that is rapidly available for dosing without the need for bridging chemotherapy. have previously reported that P-BCMA-ALLO1 demonstrates high response rates in multiple myeloma patients who • We †Day -117 have received PI, IMiDs and CD38 mAb (Dholaria et al. ASH 2023, abstract 3479). Here we demonstrate that P-BCMA- ALLO1 has promising clinical activity in patients who have received all currently available BCMA directed therapies including antibody drug conjugates, CAR-T and TCE. • P-BCMA-ALLO1 was well tolerated with no cases of DLTs or GvHD, and no instances of >Gr2 CRS or ICANS. †Day -392 • These early promising results suggest that P-BCMA-ALLO1 can fulfil the unmet medical need in a wide variety of multiple myeloma patients. • Further enrollment in the study is ongoing, with extensive biomarkers and correlative analysis to understand drivers of Where available BOR for a given regimen is indicated. †Last BCMA targeted therapy indicated relative to Day 0 of P-BCMA-ALLO1 infusion; Key: Id = Iberdomide + dex; IDd = Ixazomib + daratumumab + dex response and mechanisms of resistance. Presenting author: Bhagirathbhai.r.dholaria@vumc.org ABBREVIATIONS: Allo = Allogeneic; Auto = Autologous; BCMA = B- ll g ; 2 = 2 microglobulin; BMA = Bone marrow aspirate; CK = Cellular kinetics; CRS = Cytokine release syndrome; Cy = Cyclophosphamide; DLT = Dose limiting toxicity; ECOG = Eastern Cooperative Oncology Group; FLC = Free light chains; Flu = Fludarabine; GvHD = Graft-versus-host disease; IMiD = Immunomodulatory imide drugs; ACKNOWLEDGMENTS: The authors and Poseida Therapeutics, Inc. thank the patients, caregivers, investigators, and study site staff for their involvement in this Clinical trial identifier: NCT04960579 IMWG = International Myeloma Working Group; ITR = inverted terminal repeats; ITT = Intention-to-treat; LD = Lymphodepletion; LOD = Limit of detection; MESF = Molecules of Equivalent Soluble Fluorochrome; MHC = Major histocompatibility complex; MM = Multiple myeloma; MTD = Maximum tolerated dose; PI = proteosome inhibitors; PR = Partial response; RRMM = Relapsed and Refractory Multiple Myeloma; study. This study was sponsored and funded by Poseida Therapeutics (San Diego, CA). Study sponsored by Poseida Therapeutics sCR = Stringent Complete Response; TCE = T cell engager; TSCM = Stem cell memory T cells; VGPR = Very Good Partial Response

Exhibit 99.2

CT070 Solid Tumor Patients Require Higher Cyclophosphamide Dose than Multiple Myeloma Patients to Achieve Adequate Lymphodepletion Necessary to Enable Allogeneic CAR-T Expansion Sabrina Haag, Jeff D. Eskew, Katherine McArthur, Joanne McCaigue, Sepideh Vaziri, Samuel DePrimo, Christopher E. Martin, Catherine Gregovics, Ann Murphy, Ellen Christie, Marcela Martinez-Prieto, Rajesh Belani, Stacey Cranert, Julia Coronella, Devon J. Shedlock Poseida Therapeutics Inc., San Diego CA Design of two phase 1 studies evaluating the safety of CY1000 improves depth of lymphodepletion in multiple Lymphodepletion with CY500 did not improve CAR-T BACKGROUND Poseida’s T -rich allogeneic CAR-T cells myeloma & solid tumor patients cell expansion in P-MUC1C-ALLO1 patients SCM Poseida Therapeutics is developing innovative allogeneic T stem cell memory-rich CAR-T CAR-T infusion on day 0 Follow up, potential for redosing P-BCMA-ALLO1 P-MUC1C-ALLO1 P-BCMA-ALLO1 P-MUC1C-ALLO1 therapeutics for both hematologic malignancies and solid tumors. These include P-BCMA-ALLO1 which targets BCMA for multiple myeloma, and P-MUC1C-ALLO1 targeting MUC1-C Conditioning A B A B SCREENING FOLLOW UP for epithelial-derived solid tumors. Chemotherapy Nadir AUC Nadir AUC Cmax Cmax Cyclophosphamide (300, 500, or 1,000 mg/m2) Long-term Optimal lymphodepletion for allogeneic cell therapies remains to be established. Most P = 0.0003 P = 0.0024 P = 0.0074 P = 0.0612 P = 0.0073 P = 0.1543 3.0 42 3.0 42 106 106 and Fludarabine (30 mg/m2) on days -5, -4, -3 follow-up allogeneic CAR-T clinical trials have focused on hematologic malignancies, where patients 2.5 36 2.5 36 5 5 have likely undergone hematopoietic stem cell transplantation and are, therefore, ) L ) 10 10 30 30 lymphodepletion experienced in contrast to solid tumor patients. Consequently, solid P-BCMA-ALLO1 P-MUC1C-ALLO1 / µ 2.0 /µL / µL) 2.0 / µL) DNA DNA 3 3 3 3 tumor patients treated with allogeneic CAR-T may require higher doses of conditioning 10 24 0 0 24 104 104 x 1.5 x10 x 1 1.5 x 1 KEY INCLUSION CRITERIA: KEY INCLUSION CRITERIA: chemotherapy to achieve lymphodepletion depth comparable to patients with ( ( 18 ( ( 18 ies/µg ies/µg • RRMM as defined by the IMWG • Advanced or metastatic epithelial-derived solid C p 103 p 103 hematologic malignancies. 1.0 BC 1.0 BC • Must have received PI, IMiDs & CD38 mAb or tumor with measurable disease per RECIST v1.1 WB 12 12 WBC W W Co Co be triple refractory • Refractory to standard of care treatment or 0.5 6 0.5 6 102 102 This retrospective analysis sought to compare lymphodepletion characteristics and CAR-T • ECOG 0 or 1 ineligible/refused other existing treatment options 101 101 cellular kinetics with multiple cyclophosphamide doses across our two phase 1 trials PRIMARY ENDPOINTS PRIMARY ENDPOINTS 0.0 0 0.0 0 • Assess safety and MTD based on DLT • Assess safety and MTD based on DLT 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 (NCT05239143/NCT04960579) which are enrolling solid tumor and multiple myeloma 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 3 5 0 3 5 0 3 5 0 3 5 0 3 5 0 3 5 0 Y Y 1 Y Y 1 Y Y 1 Y Y 1 Y Y 1 Y Y 1 patients, respectively. SECONDARY OBJECTIVES SECONDARY OBJECTIVES C C Y C C Y C C Y C C Y C C Y C C Y C C C C C C • Evaluate the anti-myeloma effect of P-BCMA-ALLO1 • Evaluate the anti-tumor effect of P-MUC1C-ALLO1 • Study effect of cell dose & LD regimen to guide dose • Study effect of cell dose & LD regimen to guide dose CY300 CY500 CY1000 CY300 CY500 CY1000 Figure 2 selection for pivotal studies selection for pivotal studies Number of subjects 8 5 6 Number of subjects 5 11 3 CY1000 produces deeper lymphodepletion compared to CY300 for P-BCMA-ALLO1 (A) and P-MUC1C- Proprietary, non-viral approach to produce T -rich, LD arms and number of dosed subjects: LD arms and number of dosed subjects: ALLO1 (B) patients as demonstrated by lower WBC nadir. A. WBC nadir and AUC for the treatment window Mean 171 6,090 152,554 Mean 692 31 2,940 SCM 2 2 Std. Deviation 246 7,569 234,264 Std. Deviation 1,531 58 4,717 • Arm S (CY 300 mg/m ), n=22 • Arm A/B (CY 300 mg/m ), n=19 fully allogeneic CAR-T from healthy donors • Arm P1 (CY 500 mg/m2), n= 13 • Arm P1 (CY 500 mg/m2), n= 11 from day 0 to the day 10 visit were trending lower for P-BCMA-ALLO1 patients treated with CY500 • Arm P2 (CY 1000 mg/m2), n=7 • Arm P2 (CY 1000 mg/m2), n= 3 compared to CY300. B. No reduction of WBC nadir and AUC was observed for P-MUC1C-ALLO1 patients Figure 4 Data cutoff: Jan 4th, 2024 Data cutoff: Feb 21st, 2024 treated with CY500 compared to CY300. This indicates that CY1000 is required to produce comparable Cellular kinetics in P-BCMA-ALLO1 (A) or P-MUC1C-ALLO1 (B) patients presented by cyclophosphamide lymphodepletion between solid tumor patients and multiple myeloma patients. All patients received the 6 dose level. Peak expansion (Cmax) is shown for patients infused with a single cell dose of ~2 x 10 cells/kg. same fludarabine dose. 2 500 mg/m cyclophosphamide as part of lymphodepletion regimen did not improve P-MUC1C-ALLO1 piggyBac® Gene Insertion T -rich and versatile allogeneic CAR-T cell platform expansion in solid tumor patients. Cellular kinetics have been assessed by qPCR measuring transposon SCM copies per µg DNA. All patients received the same fludarabine dose. Transposon Design Peak IL-15 was increased & C delayed in both solid tumor Insulator Insulator • Preferentially P-BCMA-ALLO1 P-MUC1C-ALLO1 max ITR Promoter Poly(A) ITR transposes naïve T and multiple myeloma patients with CY1000 PiggyBac transposon TTAA TTAA cells resulting in T system inserts transgene SCM CONCLUSIONS rich product encoding BCMA- or Safety Switch CAR Molecule Selection Gene • Large cargo capacity anti-MUC1-C MUC1C-directed CAR piggyBac piggyBac delivers CAR, inducible scFv-CAR DNA Transposon RNA Transposase anti-B P-BCMA-ALLO1 ITR CARGO ITR safety switch, and MUC1 • Solid tumor patients had numerically higher WBC counts prior to conditioning VH-selectable marker in single step chemotherapy than multiple myeloma patients. “Cut and Paste” BCMA A Cmax Tmax AUC Genomic DNA 2 2 2 ITR CARGO ITR MUC1-C • Increasing CY dose from 300 mg/m to 500 mg/m or 1,000 mg/m for P-BCMA-ALLO1 P = 0.0086 P = 0.0205 P = 0.0010 300 12 2000 patients enhanced lymphodepletion depth leading to improved CAR-T cell expansion. Additional platform features 250 10 1600 2 2 ) L • In contrast, for P-MUC1C-ALLO1 patients, increasing CY from 300 mg/m to 500 mg/m 200 y 8 m TCR KO MHC I-KO /mL) Da / 1200 did not improve LD depth and there was no improvement in CAR-T cell expansion for g 2 2 (p 150 y 6 (pg patients treated with CY 500 mg/m compared to those treated with CY 300 mg/m . Cas-CLOVER Gene Editing Safety Selection 800 switch marker 15 15 Multiple myeloma Epithelial-derived solid tumor—100 Stud 4—IL IL • P-MUC1C-ALLO1 patients treated with CY 1000 mg/m2 demonstrated improved 400 2 50 2 lymphodepletion compared to those treated with CY 300 mg/m . There was a trend Left gRNA Clo051 2 • High editing efficiency in 0 0 0 towards improved P-MUC1C-ALLO1 expansion in patients receiving CY 1000 mg/m High fidelity gene editing resting T cells results in 0 0 0 0 0 0 0 0 0 compared to those who received CY 300 mg/m2. system used to address 5’ 3’ P-MUC1C-ALLO1 patients presented with higher baseline 0 0 0 0 0 0 0 0 0 high % of TSCM 3 5 0 3 5 0 3 5 0 Y Y 1 Y Y 1 Y Y 1 graft vs. host and host 3’ 5’ C C Y C C Y C C Y vs. graft alloreactivity • Low to no off target WBC counts & achieved comparable lymphodepletion to C C C cutting • CAR-T cell product attributes are unlikely responsible for the distinct LD requirement Right gRNA • Edits include TCR and P-BCMA-ALLO1 patients only at CY1000 P-MUC1C-ALLO1 for the two patient populations because P-BCMA-ALLO1 cells and P-MUC1C-ALLO1 B2M (MHC I) knockouts cells utilize the same transposon, gene editing and manufacturing techniques and both dCas9 dCas9 Madison et al., Molecular Therapy – Nucleic Acids, 2022. (https://www.sciencedirect.com/science/article/pii/S216225312200155X) A B B products are produced using the same screened, healthy donor pool. Cmax Tmax AUC Baseline WBC counts CY300: Nadir CY500: Nadir CY1000: Nadir P = 0.0467 0.0069 0.0019 • A major difference between these two patient populations is the prior exposure of P = P = 300 12 2000 multiple myeloma patients to lymphodepleting chemotherapy associated with prior P = 0.0025 P =<0.0001 P = 0.0047 P = >0.9999 12 3.0 3.0 3.0 250 10 CAR-T therapy or hematopoietic stem cell transplantation. 1600 10 2.5 2.5 2.5 L) ) High-yield Clinical Manufacturing ) 200 y 8 µL /m 1200 • Preliminary data suggest that solid tumor patients may require higher CY doses to / 8 /µL) 2.0 /µL) 2.0 /µL) 2.0 gDa 3 3 3 3 p 0 0 0 150 y 6 (pg/mL achieve adequate LD to enable allogeneic CAR-T expansion. 10( d 6 x1 1.5 x1 1.5 x1 1.5 u 800 Manufacturing (x ( ( ( 15 t 15 C —100 S 4—T Cell Isolation I L IL • Continued evaluation of LD regimen is needed as part of developing investigational 4 1.0 1.0 1.0 • Production process 400 Allogeneic Non-viral Gene Editing WB WBC WBC WBC 50 2 allogenic CAR-T in solid tumors. preserves TSCM manufacturing process CAR-T Cell Selection and 2 0.5 0.5 0.5 Expansion phenotype 0 0 0 enhanced with Booster Molecule technology • Nearly all CAR-carrying 0 0.0 0.0 0.0 Purification 0 0 0 0 0 0 0 0 0 ONE cells 0 0 0 0 0 0 0 0 0 B M B M B M B M 3 5 0 3 5 0 3 5 0 LEUKOPAK Fill/finish Y Y 1 Y Y 1 Y Y 1 HEALTHY DONOR C C Y C C Y C C Y ACKNOWLEDGEMENTS • “On demand” Delivery Figure 1 C C C Storage in inventory ~100 DOSES A. Baseline WBC counts prior to conditioning chemotherapy and CAR-T infusion are higher for solid tumor Figure 3 patients (n=33) receiving P-MUC1C-ALLO1 compared to multiple myeloma patients (n=42) receiving P-BCMA- P-BCMA-ALLO1 (A) and P-MUC1C-ALLO1 (B) patients treated with CY1000 compared to CY300 showed The authors and Poseida Therapeutics, Inc. thank the patients, caregivers, investigators, ALLO1. B. Post-lymphodepletion median WBC nadir was lower at CY300 and CY500 doses for P-BCMA-ALLO1 increased IL-15 levels as demonstrated by increased C and AUC in the window between Day 0 to Day max and study site staff for their involvement in this study. This study was sponsored and patients compared to P-MUC1C-ALLO1 patients. Both groups achieved similar deep WBC nadir when 10. The IL-15 C was also delayed in patients receiving CY1000 as compared to the lower CY groups. All max funded by Poseida Therapeutics (San Diego, CA). receiving CY1000. All patients received the same fludarabine dose. B = P-BCMA-ALLO1; M = P-MUC1C-ALLO1. patients received the same fludarabine dose. Presenting author: shaag@poseida.com ABBREVIATIONS: AUC = Area under the curve; BCMA = B-cell maturation antigen; B2M = 2 microglobulin; CK = cellular kinetics; CY = cyclophosphamide; DLT = Dose limiting toxicity; ECOG = Eastern Cooperative Oncology Group; TCR KO = T cell receptor gene knock out; IL-15 = interleukin 15; IMiD = Immunomodulatory imide drugs; IMWG = International Myeloma Working Group; ITR = inverted terminal repeats; LD = Lymphodepletion; MHC I = Major histocompatibility complex class I; MTD = maximum tolerated dose; MUC1 = Mucin 1; MUC1-C = Mucin 1, C-terminal domain; Clinical trial identifier: NCT04960579/NCT05239143 PI = proteasome inhibitor; RRMM = Relapsed/Refractory Multiple Myeloma; TSCM = stem cell memory T cells; TTAA = thymine-thymine-adenine-adenine nucleotide sequence; WBC = white blood cells. STATISTICAL ANALYSIS: Mann-Whitney test (Figure 1), Kruskal-Wallis test with Dunn’s multiple comparisons test shown (Figures 2 – 4), median with range is shown in all graphs. Study sponsored by Poseida Therapeutics

Exhibit 99.3