NASDAQ: SABS

Our proprietary platform holds the potential to generate additional novel therapeutic candidates to expand our pipeline, utilizing the human immune response to generate the optimal repertoire of hIgG for drug targets of interest. Our drug development production system is able to generate a diverse repertoire of specifically targeted, high-potency, hIgGs that can bind to multiple sites on targeted immunogens, making them ideally suited to address the complexities associated with many immune-mediated disorders and address a wide range of serious unmet needs in human diseases.

Our Development Pipeline: Advancing a Pipeline in Autoimmune Diseases Led by SAB-142

The following table highlights our current development pipeline:

SAB-142: Our Lead Product Candidate

Our wholly owned lead product candidate, SAB-142 is a potentially disease-modifying, redosable immunotherapy in clinical development for the treatment of autoimmune type 1 diabetes (T1D). SAB-142 is a multi-specific, fully human anti-thymocyte globulin (hATG) with a mechanism of action analogous to that of rabbit ATG (rATG). rATG has demonstrated in multiple clinical trials the ability to slow disease progression in patients with new- or recent-onset of Stage 3 T1D. SAB-142, like rATG, directly targets multiple immune cells involved in destroying pancreatic beta cells, including modulation of “bad

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acting” T-lymphocytes. By stopping immune cells from attacking beta cells, this treatment has the potential to preserve insulin-producing beta cells. The mechanism of action of SAB-142 has been clinically validated in numerous clinical trials with a rabbit anti-thymocyte globulin (rATG). In addition, data from approximately 800 human subjects have been treated with antibodies produced by our platform, including in the Phase 1 study of SAB-142, where we have seen no incidence of serum sickness and neutralizing anti-drug antibodies (ADAs). We expect this finding to continue through the clinical development of SAB-142.

There is an established regulatory path for T1D indications using the SAB-142 modality. Our regulatory pathway has also been established with the United States Food and Drug Administration (FDA), the United Kingdom Medicines and Healthcare products Regulatory Agency (MHRA), and the Therapeutic Good Administration (TGA) in Australia. The FDA regulates polyclonal hIgG and mAbs differently, as mAbs are regulated through the Center for Drug Evaluation and Research (CDER) while pAbs are regulated by the Center for Biologics Evaluation and Research (CBER). CBER has approved more than 30 immunoglobulin products from both human- and animal-derived plasma. Further, CBER is very familiar with our production platform and pAb products. We have navigated three SAB drug products through seven clinical trials with one product having advanced to Phase 3, building our safety database as well as positive efficacy data. As our lead program SAB-142 advances, we intend to expand our pipeline in complementary indications through strategic utilization of our platform.

We received an Investigational New Drug (IND) clearance from the FDA in May 2024 and announced positive topline data from our Phase 1 clinical trial of SAB-142 in January 2025 and December 2025. We initiated our registrational Phase 2b clinical trial, called the SAFEGUARD study, in Q3 2025 and dosed the first patient in December 2025. In May 2025, SAB confirmed its intent with the FDA to utilize the data from the SAFEGUARD study as supportive evidence for future regulatory approval.

Background On Type 1 Diabetes

High Prevalence in Type 1 Diabetes

T1D is a complex and life-threatening autoimmune disease in which the body mistakenly attacks the insulin-producing beta cells of the pancreas. Living with this disease requires daily, sometimes hourly, intensive insulin management with the potential for numerous complications. Despite improvements in glucose monitoring and insulin administrations, mortality amongst people with T1D remains up to 13 times higher compared to matched controls. From a drug development perspective, shifting away from chronic disease management and towards disease-modifying therapies has the potential to change and save millions of lives.

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According to the T1D Index, a global data simulation tool launched by Breakthrough T1D Foundation, formerly known as the Juvenile Diabetes Research Foundation (JDRF), in 2022, the prevalence of T1D has increased at four times the rate of population growth in every country across the globe since 2000.

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Nearly 1 in 300 children in the United States will be diagnosed with T1D during childhood, and one in every seven healthcare dollars can be attributable to the cost of managing diabetes over the lifetime.

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An estimated 9.5 million people were living with T1D worldwide in 2024, and this number is predicted to increase to 14.7 million by 2040.

Based on birth cohorts from 1950 to 2040, 6.85 million lives will be lost by 2040 if people are unable to access interventions to diagnose and treat T1D. According to these estimates, T1D stands to become one of the world’s largest deadly chronic health conditions, similar in scale and impact to HIV.

Current Type 1 Diabetes Treatment Landscape and Their Limitations

Despite significant advances in diabetes technology which has enabled those with T1D mellitus to manage and improve their metabolic control, there remains a significant unmet need in this therapeutic area and the patient burden and potential for acute complications remains high. Insulin injection is the current standard of care for T1D, yet self-management of T1D involves complex daily routines and careful monitoring of dietary intake and activity levels to potentially achieve glycemic targets associated with a reduced risk of long‐term diabetes complications. Insulin pumps featuring a computerized system for sensing blood glucose to deliver an appropriate dose of insulin have been frequently reported to the FDA for problems. A high incidence of failure in achieving glycemic targets is a consistently reported issue. Additionally, long term complications of the disease include a reduced life expectancy of 10-15 years, and significant acute complications such as hyperglycemia, including diabetic ketoacidosis, premature myocardial infarction, stroke, limb ischemia, gangrene, kidney failure, blindness due to diabetic retinopathy, coma and potentially death. All current therapies require patients to carefully monitor their dietary intake, which is inconvenient in adults and a frequent point of failure in adolescents and children.

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Pancreas transplantation for uncontrolled diabetes was first performed in the 1960s and established the principle that replacing the beta cells could restore physiological glucose control. Pancreas transplants are limited due to the availability of organs, complicated surgical interventions, and require lifelong immunosuppression. Despite its limitations, approximately 30,000 pancreas transplants have been performed worldwide to date.

Several existing treatment options for T2D have been investigated to treat T1D, though generally without success. While SGLT-1/2 and SGLT-2 inhibitors were initially approved in Europe and Japan with label restrictions to certain sub-groups of patients with T1D, and continue to be approved for patients with T2D, these therapies have since been withdrawn from the European market and have not received regulatory approval in the U.S. for T1D due to safety risks primarily related to the risk of diabetic ketoacidosis. Pramlintide (Symlin), an amylin peptide analog approved for mealtime injections, has been approved for use in both T1D and T2D since 2005 but has not been adopted widely.

Other therapeutic modalities, including monoclonal antibodies, are under clinical investigation and have demonstrated evidence of the potential to delay the onset of T1D. In November 2022, the FDA approved Tzield (teplizumab), a humanized anti-CD3 monoclonal antibody for the treatment of patients with two or more diabetes-related auto-antibodies to delay the onset of T1D. However, as with any autoimmune disease, a single treatment such as Tzield cannot address the entire spectrum of the unmet need of patients with Stage 1-4 T1D due to the significant heterogeneity of the disease, where every patient may not respond to the therapy. Currently, Tzield (known as Teizeild in Europe) is approved in the U.S. and in the EU for patients with Stage 2 T1D. Tzield has been filed for approval in the United States for Stage 3 T1D after receiving a Commissioner's National Priority Voucher (CNPV) under the CNPV pilot program in late 2025.

The treatment burden for Tzield for Stage 2 and Stage 3 T1D is one course of intravenous (IV) daily therapy for 14 days at Month 1 and two courses of IV daily therapy for 12 days, at Month 1 and Month 6, respectively. Teplizumab also has an immunogenicity liability. Of patients treated with Teplizumab, 57% had ADAs, 46% of which were neutralizing ADAs.

There are currently no approved therapies in delaying the progression of T1D in new onset Stage 3 T1D patients, thus significant unmet medical needs remain for the development of therapies that target specific patient needs across various stages of T1D diagnosis. New onset Stage 3 T1D is the first indication we plan to pursue with SAB-142, as we continue our work to change the lives of people impacted by T1D through unique disease-modifying therapies.

Clinical Validation of Anti-Thymocyte Globulin in New Onset Type 1 Diabetes

Maintenance of the level of connecting peptide (C-peptide), a short 31 amino acid polypeptide that connects insulin’s A chain to its B chain in the proinsulin molecule, is a validated surrogate endpoint for endogenous insulin production, essential for delaying progression of T1D. Placebo controlled trials with low-dose rATG, defined as a single dose of 2.5 milligram per kilogram (mg/kg) and 0.5 mg/kg administered intravenously over two days in an ambulatory, or outpatient setting, have shown statistically significant maintenance of C-peptide levels and thus a delay in progression of recent onset T1D.

TN-19: Low-Dose rATG Preserved C-peptide in New Onset T1D 1 and 2 Years Post Treatment

Based on the results of a Phase 2 clinical trial, TN19, conducted at the University of Florida, a single dose of rATG showed sustained benefit in T1D over a two-year period by maintaining significantly higher C-peptide levels than a placebo control. In addition to the C-peptide data, rATG treated patients showed a significant reduction in glycated hemoglobin A1C (HbA1C) over the placebo group. However, more than 65% of treated patients in this study reported serum sickness due to the infusion of a non-human antibody, with symptoms that included rash, malaise, fever, and joint swelling, with over 50% of those subjects developing serum sickness of Grade 3-4 (severe and life-threatening according to the CTCAE criteria). The symptoms often required treatment with steroids that control serum sickness but impair diabetes management and reduce the capacity to redose rATG when C-peptide levels begin to drop.

The below graph shows the statistically significant preservation of C-peptide (p=0.00005) and the reduction of HbA1C (p=0.011) at year two in low dose rATG from the TN19 study:

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Source: Haller, Michael J., et al. “Low-Dose Anti-Thymocyte Globulin Preserves C-Peptide, Reduces HbA1c, and Increases Regulatory to Conventional T-Cell Ratios in New-Onset Type 1 Diabetes: Two-Year Clinical Trial Data.” Diabetes, vol. 68, no. 6, 2019, pp. 1267–1276.

MELD-ATG: Minimal Effective Low Dose of rATG Preserved C-peptide in New Onset T1D One Year Post Treatment

In September 2025, results from the Phase 2 MELD-ATG trial were published in The Lancet. MELD-ATG was a randomized, double-blind, placebo-controlled, adaptive dose-ranging study evaluating rATG in 117 participants aged 5–25 years with new onset Stage 3 T1D (diagnosed 3–9 weeks prior to treatment).

The primary endpoint was stimulated C-peptide area under the curve (AUC) during a 2-hour mixed-meal tolerance test at 12 months. The 2.5 mg/kg dose demonstrated statistically significant preservation of C-peptide versus placebo (p=0.0028). The 0.5 mg/kg dose, identified as the minimum effective dose, also demonstrated statistically significant preservation of C-peptide versus placebo (p=0.014). At 12 months, the 0.5 mg/kg group demonstrated a statistically significant reduction in adjusted mean HbA1c versus placebo (p=0.024). The 2.5 mg/kg group showed a numerical reduction in adjusted mean HbA1c versus placebo that did not reach statistical significance. Continuous glucose monitoring metrics showed numerically higher time in range in treated participants.

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The chart below shows the statistically significant preservation of C-peptide and reduction of HbA1C over one year in the MELD-ATG study:

Source: Mathieu, Chantal, et al. “Minimum Effective Low Dose of Antithymocyte Globulin in People Aged 5–25 Years with Recent-Onset Stage 3 Type 1 Diabetes (MELD-ATG): A Phase 2, Multicentre, Double-Blind, Randomised, Placebo-Controlled, Adaptive Dose-Ranging Trial.” The Lancet, published online 18 Sept. 2025.

All treated participants experienced at least one AE (most were Grade 1 or 2). Dose-dependent AEs included cytokine release syndrome (33% at 2.5 mg/kg; 24% at 0.5 mg/kg; 0% placebo) and serum sickness (82% at 2.5 mg/kg; 32% at 0.5 mg/kg; 0% placebo). There were no deaths related to adverse events.

Safety Across Clinical Trials of rATG in New Onset T1D

A review of safety parameters based on both short and long-term safety data (up to five years from three separate clinical trials conducted with low-dose rATG in Stage 3 T1D patients) highlights that safety issues associated with dosing humans with rabbit-derived antibodies are predominantly focused on the serum sickness, high immunogenicity, and CD4+ sustained lymphodepletion. These side effects appear to be dose-dependent, with the higher dose level of rATG at 6.5mg/kg having higher proportion of participants with the AEs. Nevertheless, at low dose levels, this mechanism of action (MoA) is proven to be immunomodulatory rather than immunosuppressive. Three studies were conducted with two doses of rATG: a single trial with a 6.5 mg/kg dose, and two studies using a low dose of 2.5 mg/kg. Each trial was adequately designed, randomized, double-blind, and placebo controlled. In all three trials, extensive safety assessments and a long-term safety follow-up showed no increase in infection versus placebo, no opportunistic infections or infections known to develop predominantly in immunosuppressed patients, and no difficulty in clearing infections. The 6.5 mg/kg trial investigated an immune response to either a recall or novel antigen as a representative of an immune response to vaccination or an infection. The findings demonstrated that the administration of a single dose of rATG did not result in decreased humoral response versus placebo. Finally, none of the three trials observed an increase in liquid cancers or solid malignancies.

Limitations to Rabbit Anti-Thymocyte Globulin

Rabbit ATG shows therapeutic promise, but its heterologous nature and high immunogenicity are problematic given adverse events that could inhibit long term disease modification and redosing. It is well established that treatment with heterologous proteins such as rATG can result in serum sickness, which can trigger Grade 3 or higher adverse events. Serum sickness is

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defined as a Type 3 hypersensitivity reaction. The heterologous nature of rATG also results in the production of neutralizing ADAs in most patients even after a single course of therapy. Neutralizing ADAs, or NAbs, are a subset of ADAs that bind to the drug and inhibit its pharmacologic action or activity. Once pharmacological function is inhibited, beta cells are left unprotected from attacks by the cytotoxic CD8-positive T-cells or inflammatory mediators, and the disease continues to progress.

SAB-142: Our Proposed Solution for Type 1 Diabetes

SAB-142 is a first-in-class, human, multi-target ATG treatment designed to provide superior efficacy and safety in delaying the onset or progression of T1D and offers a novel human alternative to rabbit- or equine-derived ATG with potential for safe and reliable redosing while eliminating the treatment burden observed with currently available therapies.

While the MOA of our compound closely resembles rATG, we believe SAB-142 has demonstrated clear advantages that are fundamental for safe and reliable redosing required to delay disease progression.

Data from preclinical studies and clinical trials suggest that commercially approved rATG has been shown to transiently restore immune-tolerance and reduce autoimmune attack on pancreatic beta cells in T1D patients. Following IV administration, both rATG and SAB-142 have been shown to target key circulating immune cell types involved in an autoimmune response in T1D. Both ATGs cause a dose proportional sustained exhaustion of CD4+ and CD8+ T-cells while preserving regulatory T cells (Tregs) in addition to modulating other autoimmune pathways involved in T1D pathophysiology. By reducing overreactive CD4+ and CD8+ T cells while preserving Tregs, SAB-142 is expected to reduce autoimmune β-cell destruction to delay the onset (Stage 2) or progression (Stage 3) of autoimmune T1D.

In addition to potentially preserving beta cell function in early T1D patients, SAB-142 offers the potential of safe and reliable redosing when examining clinically meaningful indicators such as C-peptide levels and HbA1c without the potential risk of inducing major immune reactions of animal derived immunoglobulins. In the first-in-human Phase 1 clinical trial, SAB-142 demonstrated zero serum sickness and zero immunogenicity at the target dose levels, including in a cohort of redosed healthy volunteers (HV), thus supporting its potential for safe and reliable redosing.

Clinical Strategy for SAB-142

T1D is an autoimmune disease characterized by destruction of insulin producing beta-cells in the pancreas by the patient’s own immune system. Immunological processes resulting in the breakdown of self-tolerance and gradual destruction of pancreatic beta cells by the patient’s own immune system preceding the clinical onset of disease oftentimes starts very early in patients’ lives, sometimes as early as in utero. T1D affects people of all ages, with the average age of diagnosis at 13 years old. Stage 1 is the start of T1D, marked by individuals having two or more diabetes-related autoantibodies and still normal blood sugar concentrations. In Stage 2, individuals have dysglycemia but without symptoms. Stage 3 is the time of a full clinical diagnosis. Unfortunately, when an individual is first diagnosed with clinical stage T1D, 50-90% of pancreatic insulin-producing beta cells are already destroyed. Hence, it is critical to start therapy that preserves the remaining fully functional beta cells as soon as possible as it may provide the highest benefit throughout the patient’s lifetime. The table below illustrates the therapeutic landscape of T1D and its disease continuum.

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T1D Disease Continuum

As referenced in the above illustration, one of the early proposed studies in our clinical development program will be in those patients with newly diagnosed Stage 3 T1D. Following the trials in Stage 3, we would progress into clinical trials in Stage 2 patients. Stage 2 patients are those who do not yet have a full clinical onset of T1D and have functional beta cells that can be further preserved. In this patient population, we will aim to delay the onset of Stage 3 clinical T1D along with evaluation of the redosing potentially aimed at fully preventing clinical onset of disease. The ultimate vision for SAB-142 is founded on the potential ability to safely redose by delivering a consistent and effective dose of this medication twice per year to fully halt progression of established clinical disease or delay its onset indefinitely.

Clinical Development of SAB-142

On January 28, 2025, we announced positive topline Phase 1 clinical results with the Company’s potentially disease-modifying T1D therapy SAB-142. Based on the data, we advanced SAB-142 into a registrational Phase 2b trial, SAFety and Efficacy of human anti-thymocyte immunoGlobUlin SAB-142 ARresting progression of type 1 Diabetes (SAFEGUARD), in Q3 2025 to evaluate the therapeutic candidate in adult, adolescent, and pediatric patients with new onset, Stage 3 T1D.

We shared additional Phase 1 clinical trial results on December 17, 2025.

SAB-142 Phase 1 HUMAN Clinical Data

The SAB-142 Phase 1 HUman anti-thymocyte biologic in first-in-MAN(HUMAN) clinical trial was designed as a randomized, double-blind, placebo-controlled, single-ascending dose, adaptive design clinical study among HV and one cohort of participants with T1D that commenced dosing in November 2023. The objectives include establishing safety, tolerability, pharmacokinetic (PK), immunogenicity, and pharmacodynamic (PD) profile for SAB-142.

The reported topline results showed the following outcomes in HV cohorts and a redosed HV cohort:

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Favorable safety profile: SAB-142 was well-tolerated in both HV and T1D patients. SAB-142 demonstrated a safety profile superior to rabbit anti-thymocyte immunoglobulin (rATG) as the data from the Phase 1 trial confirmed SAB-142 does not cause serum sickness (0%, N=0/68) and there were no adverse events (AEs) associated with anti-drug antibodies (ADAs; 0%, N=0/68) at any dose in any cohort, including in the redosed HVs and T1D patient cohort. In all treated participants, there were no drug-related serious adverse events (SAE). Most AEs were mild and associated with day 1-2 infusions, with only Grade 1 flu-like symptoms and transient

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infusion-site reactions including pruritus and tenderness. The most common AE was headache, which is consistent with typical AEs for T-cell modifying therapies.

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Demonstrated sustained “T-cell exhaustion” signature: SAB-142 demonstrated PD activity consistent with its intended mechanism of action, including induction of inhibitory receptor expression associated with CD4+ T conventional (“Tconv”) cell exhaustion. Tconv cells are a subset of helper T lymphocytes that play a central role in coordinating immune responses. In T1D, autoreactive T cells contribute to immune mediated destruction of pancreatic beta cells resulting in progressive loss of endogenous insulin production.

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PD-1+ Tconv Cells: PD-1+ Tconv cells are a type of immune cell that carry a protein called PD-1 on their surface. PD-1 acts as a natural brake on the immune system. When PD-1 levels increase, the activity of these immune cells is reduced. In T1D, certain immune cells attack insulin producing beta cells in the pancreas. When CD4+ Tconv cells express higher levels of PD-1, they become less aggressive and less likely to damage tissue. This state is often referred to as T-cell exhaustion. An increase in PD-1+ Tconv cells after treatment suggests that the immune response may be more controlled. In autoimmune diseases such as T1D, this effect may potentially help slow the destruction of beta cells. As shown in graph below titled “Relative PD-1+ Tconv Cells ± SEM,” treatment with SAB-142 was associated with an increase from baseline in the percentage of PD-1–expressing CD4+ Tconv cells compared to placebo. Following infusion, SAB-142 treated participants exhibited a sustained elevation in PD-1+ Tconv cells over the 120 day period, whereas placebo treated participants remained near baseline levels. The separation between treatment and placebo arms was evident beginning in the early post dose period and persisted through Day 120 supporting target engagement and downstream immunomodulatory activity.

Relative PD-1 + Tconv Cells ± SEM

Note: SAB-142: combined 1.5 mg/kg and 2.5 mg/kg dosed cohorts.

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TIGIT+ Tconv Cells: Similar to PD-1, TIGIT is a protein found on the surface of certain CD4+ Tconv immune cells and also functions as a natural brake on the immune system. When TIGIT levels increase, the activity of these immune cells is reduced. In T1D, where immune cells attack insulin producing beta cells in the pancreas, higher TIGIT expression on CD4+ Tconv cells is associated with a less aggressive immune response. This reduced activity is also consistent with T-cell exhaustion. An increase in TIGIT+ Tconv cells after treatment suggests that the immune response may be more controlled and may potentially help reduce beta cell destruction. As shown in the graph titled “Relative TIGIT+ Tconv Cells ± SEM,” treatment with SAB-142 was associated with an increase from baseline in the percentage of TIGIT expressing CD4+ Tconv cells compared to placebo. Following infusion, SAB-142 treated participants exhibited sustained elevation in TIGIT+ Tconv cells over the 120 day period, whereas placebo treated

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participants remained near baseline levels. The separation between treatment and placebo arms was observed during the post dose period and persisted through Day 120 supporting PD activity consistent with immune modulation.

Relative TIGIT+Tconv Cells ± SEM

Note: SAB-142: combined 1.5 mg/kg and 2.5 mg/kg dosed cohorts.

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CD4+ Tconv Cell Dual Exhaustion Markers: In addition to looking at PD-1 or TIGIT alone, we also measured CD4+ Tconv cells that express two inhibitory proteins at the same time. When CD4+ Tconv cells express combinations such as PD-1 and TIGIT, PD-1 and KLRG1, or KLRG1 and TIGIT, this suggests a deeper level of immune restraint than expression of a single marker alone. Co-expression of these inhibitory proteins is commonly associated with a more exhausted and less active T cell state. As discussed above for PD-1+ and TIGIT+ Tconv cells, higher levels of these inhibitory markers indicate that the immune response may be more controlled. An increase in dual positive Tconv cells after treatment further supports the induction of CD4+ Tconv cell exhaustion. In the context of T1D, this pattern is consistent with reduced immune driven attack on insulin producing beta cells. As presented in the illustration below titled “Tconv Median % Change from Baseline (PD-1/KLRG1, PD-1/TIGIT, KLRG1/TIGIT),” SAB-142–treated participants demonstrated greater median percent increases from baseline in dual positive CD4+ Tconv subsets compared to placebo across multiple time points (Days 30, 45, 90, and 120). The magnitude and persistence of dual marker expression were consistent with enhanced induction of an exhausted phenotype in effector T cells.

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Tconv Median % Change from Baseline (PD-1/KLRG1, PD-1/TIGIT, KLRG1/TIGIT)

Note: SAB-142: combined 1.5 mg/kg and 2.5 mg/kg dosed cohorts.

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Preserved and activated regulatory Tregs: Phase 1 PD data demonstrated that SAB‑142 preserved Tregs while simultaneously inducing markers consistent with Treg activation, an immunologic profile aligned with disease‑modifying potential in Type 1 Diabetes. The graph below demonstrates that Tregs remained stable relative to baseline with no meaningful decline observed through Day 120, indicating that SAB‑142 does not deplete this regulatory subset. Instead, SAB‑142 treatment results in the preservation of Tregs in the 1.5 mg/kg and 2.5 mg/kg dose cohorts in HV.

Note: SAB-142: combined 1.5 mg/kg and 2.5 mg/kg dosed cohorts.

Additionally, SAB‑142 induces expression of the inhibitory receptor TIGIT on Tregs, a recognized marker of Treg activation that may enhance suppressive immune function in HV. The graph below shows that SAB‑142 increases the proportion of TIGIT+ Tregs over time, whereas placebo remains relatively unchanged. Across day 120, the SAB‑142 cohort trends consistently above pre‑infusion baseline with values gradually rising and peaking around Day 90 before stabilizing.

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Note: SAB-142: combined 1.5mg/kg and 2.5mg/kg dosed cohorts.

TIGIT+ Tregs acts as a beneficial PD signal potentially contributing to restoration of immune tolerance and improved regulation of effector T‑cell activity implicated in beta cell destruction. Across datasets, Tregs exhibit stability, lack of cytotoxic loss, and activation in response to SAB‑142. These findings support the mechanistic hypothesis that SAB-142 may modulate the autoimmune environment without triggering broad immunosuppression, while maintaining T cell regulatory capacity and promoting exhausted CD4+ T cell profiles associated with C-peptide preservation.

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Transient lymphopenia supports maintenance dosing: Lymphocytes are white blood cells that help regulate immune responses. Monitoring these levels helps evaluate how a treatment affects overall immune cell counts. Transient lymphopenia, an on-target marker of target engagement and PD activity, was observed in all subjects (100%; N=68) following the induction dose with lymphocyte counts returning to baseline within 1 to 3 days. This pattern was also seen after the second administration in the HV cohort (100%; n=8). As shown in the graph titled “Mean Absolute Lymphocytes ± SEM Normalized to Original Pre-SOI in HV,” lymphocyte levels decreased shortly after dosing and then rapidly returned to pre dose levels. Unlike certain immunomodulatory therapies that deplete lymphocytes for extended periods of up to two years, SAB-142 did not demonstrate sustained lymphodepletion. The rapid recovery of lymphocyte counts suggests immune modulation without prolonged suppression and supports the potential for repeat dosing and maintenance administration at six month intervals.

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Mean Absolute Lymphocytes ± SEM Normalized to Original Pre-SOI in HV

SAFEGUARD: Multicenter, Global Phase 2b for SAB-142 in Stage 3 Type 1 Diabetes Patients

Based on the completed Phase 1 clinical trial, we initiated a global Phase 2b study called SAFEGUARD to assess the safety, efficacy, and tolerability of SAB-142 in patients with Stage 3 new onset T1D. SAFEGUARD, the Company’s multicenter, global, randomized, double-blind, placebo-controlled Phase 2b clinical trial, is designed and powered as a registrational program across multiple regions, including the United States, EMA-member states, the United Kingdom, Australia, and New Zealand.

SAFEGUARD, as shown below, would enroll 159 pediatric, adolescent, and adult participants aged 5–40 years with new onset Stage 3 T1D within 100 days of diagnosis and baseline C-peptide ≥200 pmol/L. The study consists of Part A, a 12 patient cohort, and Part B, a 147 patient randomized cohort evaluating two active dose levels of SAB-142, 1.5 mg/kg and 2.5 mg/kg vs. placebo administered intravenously using a split two-day dosing regimen, with a second dose at Month 6. The primary efficacy endpoint of the Phase 2b trial is stimulated C-peptide following a 2-hour Mixed Meal Tolerance Test (MMTT) at 12 months, powered to detect at least a 40% difference with 80% power. Key secondary and other endpoints include HbA1c, Time in Tight Range, Time in Range, Time Above and Below Range, insulin use, hypoglycemic episodes, and other safety assessments. These endpoints are structured to evaluate the potential of SAB-142 to preserve beta cell function and modulate the underlying autoimmune activity responsible for T1D progression.

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SAFEGUARD: Global Phase 2b Study Design

All participants, including placebo, who complete the blinded portion of SAFEGUARD Part B are eligible to enroll into Part C, a 12-month long-term extension (LTE). Part C of SAFEGUARD is designed to evaluate the maintenance phase safety and efficacy of SAB‑142 over a 24‑month treatment period where all individuals receive active treatment to support long‑term assessment of durability, redosing feasibility, and extended safety monitoring. Part C enables the Company to collect efficacy and safety data up to 24 months, including redosing safety, maintenance PD activity, and extended metabolic outcomes. In addition to supporting a more robust safety database, Part C provides continuity for sites and participants after completion of Part B and enhances the probability of regulatory approval by contributing multi‑dose, long‑duration exposure data.

The Phase 2b study’s global design, registrational powering, and comprehensive metabolic and immunologic endpoints are intended to support potential future regulatory submissions. On May 29, 2025, the Company held a constructive Type B meeting with the FDA. The meeting followed positive topline data from a Phase 1 single-ascending dose trial in healthy volunteers for SAB-142. The primary discussion centered on questions related to all aspects of SAB-142’s Phase 2b SAFEGUARD clinical trial design and chemistry, manufacturing, and controls processes. The FDA provided clear, constructive, and actionable guidance during the discussion leading to alignment on the design and advancement of our Phase 2b SAFEGUARD study. SAB confirmed its intent with the FDA to utilize the data from this study as primary evidence for future regulatory approval. Although, while our ongoing Phase 2b study is designed to provide robust evidence of safety and efficacy, the FDA may require additional supportive clinical trial(s) beyond this study to establish substantial evidence sufficient for BLA approval.

The study was initiated in Q3 2025 and the first patient was dosed in December 2025. Global trial startup activities are underway and study is actively enrolling and dosing patients at multiple global sites with topline data expected in the second half of 2027.

In addition, our clinical development efforts are supported by global T1D research organizations, including INNODIA, the Australasian Type 1 Diabetes Immunotherapy Collaborative, Breakthrough T1D, UK T1D Research Consortium, and specialized clinical research networks such as AK Clinical Research. Collectively, these partnerships reflect our strategy to conduct SAB‑142 development alongside leading T1D scientific and clinical experts around the world, integrating academic leadership into study design, patient engagement, and scientific interpretation.

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Other Immunology Indications

T- and B-cells are multifunctional lymphocytes whose dysregulation was shown to have a central role in the pathogenesis of more than 80 autoimmune diseases, including T1D, systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), multiple sclerosis (MS), and celiac disease. The therapeutic success to date of lymphocyte-mediating therapies in a variety of autoimmune diseases and our in vivo and in vitro pre-clinical and Phase 1 work from SAB-142 in T1D supports direct progression into Phase 2 in other autoimmune indications.

Proprietary Production Platform Overview

Our proprietary production platform gives us the unique ability to generate targeted, hIgG without the need for human donors or plasma. Diverse and high-potency hIgG can be targeted to human immunogens for immune disorders or cancer, viruses, bacteria, and toxins. The production system relies on advanced genetic engineering that functionally replaces bovine immunoglobulin with hIgG (resulting in our Tc Bovine) produced from the full germ-line repertoire of human antibody heavy chain and kappa light chain genes on an engineered human artificial chromosome (HAC). The human antibody genes have been further engineered to efficiently produce a diverse repertoire of hIgG in bovine B-cells in response to specifically targeted immunogens as a result of the hyperimmunization of the Tc Bovine. Bovine were selected because they are large animals that produce large amounts of plasma, and as ruminants, have high concentrations of circulating hIgG with a robust response to immunogen challenge that produces high potency, high avidity hIgG.

Through our production platform, we have engineered a targeted hIgG production platform that emulates the way that the human immune system synergistically targets the complexity of human disease. The discovery, development, and production process represents a “plug-and-play” approach:

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Develop Immunogen for Disease Target. An immunogen is developed for a specific target in much the same that human vaccines are developed. The production platform is designed to address virtually any target including bacteria (whole killed), viruses, toxins, nucleic acids (i.e., RNA and DNA vaccines), whole cells, and human tissues.

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Hyperimmunize Tc Bovine. Tc Bovine are genetically engineered to produce hIgG. They are then hyperimmunized with the desired immunogen, driving the immune response beyond protective levels that have been shown in some cases to be 40-60 times more potent than hIgG produced in convalescent patients.

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Collect Plasma. The target specific hIgG is collected from the Tc Bovine by plasma donations.

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Isolate hIgG. hIgG is then isolated from the plasma through a well-established plasma fractionation and purification process and Quality Control tested. This highly purified hIgG is then ready for use as a human immunotherapy treatment or prophylactic.

Our production platform is replicable and scalable given Tc Bovine are genetic clones. Animals can be produced through cloning technology and the plasma fractionation process scaled to meet market demand through a well-established GMP process. We believe that targeted hIgG can be produced against the same immunogen or multiple immunogens, depending on the disease target and indication, in as many Tc Bovine as necessary to generate sufficient doses to fully supply the target market. Consistency of hIgG product is achieved by testing the potency of hIgG contained in each plasma collection and then combining plasma collections in a manufacturing pool that generates specified potencies within a specified antibody protein concentration.

Manufacturing Strategy

In support of our operations, we currently operate two plasma fractionation and purification facilities in Sioux Falls, South Dakota: a 50L small batch scale cGMP suite that has produced clinical grade drug product to accommodate Pre-Clinical and Phase 1 studies, and a 200L scale larger batch cGMP suite that was completed in 2021 which can be used to produce clinical grade drug product to accommodate larger sized advanced Phase 2 clinical studies or Emergency Use scale. As we continue to scale our manufacturing process and capabilities around the advancement of our SAB-142 program, we will begin expanding our manufacturing footprint and adding manufacturing redundancy with a Contract Development and Manufacturing Organization (CDMO) for producing late-stage clinical drug supply and commercial drug product.

In addition, we continue to maintain supportive laboratory facilities and operations in Sioux Falls, South Dakota, for drug discovery, product and process development, and clinical manufacturing. We have fully GLP and cGMP compliant quality control testing facilities and we have further developed our own internal antigen (immunogen) discovery and production capabilities to accommodate the Tc Bovine immunizations that improve our overall plasma production speed and efficiency further enhancing our drug discovery and scaled clinical manufacturing timeline. We recently completed an expansion of our

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research and development laboratory facilities to accommodate our discovery programs, support for our pre-clinical pipeline programs, and process development research for our clinical drug product candidates.

Our Tc Bovine are housed at dedicated specialty facilities, accredited by the American Association for Accreditation of Laboratory Animal Care (the “AAALAC”) that cater to the production, health, safety, and welfare of the animals, and provide plasma production. The upstream process is scalable. Animals donate plasma three times per month (up to 2.4% of bodyweight each time). To produce more product, more animals are added to the program and immunized to the target. To support the continued scaling of our SAB-142 program and the implementation of a robust risk‑mitigation strategy, we are expanding our Tc Bovine capacity by establishing a second, redundant animal facility at a separate location.

Competition

The biopharmaceutical industry is highly competitive and subject to rapid and significant technological change as research provides a deeper understanding of the pathology of diseases and new technologies and treatments are developed. We believe our scientific knowledge, technology, and development capabilities provide us with substantial competitive advantages, but we face potential competition from multiple sources, major pharmaceutical, specialty pharmaceutical and existing or emerging biotechnology companies, academic research institutions, governmental agencies, and public and private research institutions worldwide. We consider the following companies to be among our competitors or future competitors: Sanofi S.A., Sana Biotechnology, Imcyse, vTv Therapeutics, Century Therapeutics, IM Therapeutics, Sernova, and Biomea Fusion.

Our competitors may have significantly greater financial resources, robust drug pipelines, established presence in the market and expertise in research and development, manufacturing, pre-clinical and clinical testing, obtaining regulatory approvals and reimbursement and marketing approved products than we do. These competitors also compete with us in recruiting and retaining qualified clinical, regulatory, scientific, sales, marketing, and management personnel, in establishing clinical trial sites and patient registration for clinical trials, as well as in acquiring technologies complementary to, or necessary for, our programs. Smaller or early-stage companies may also prove to be significant competitors, particularly through collaborative arrangements with large and established companies.

If any future product candidates identified through our current lead programs are eventually approved for sale, they will likely compete with a range of treatments that are either in development or currently marketed for use in those same disease indications. Our success will partially depend on our ability to obtain, maintain, enforce, and defend patents and other intellectual property rights with respect to our hIgG that are proven to be safer or more effective or are less expensive than competing products. We could see a reduction or elimination in our commercial opportunity if our competitors develop and commercialize drugs that are safer, better tolerated, more effective, more convenient to administer, less expensive, more resistant to viral escape, or receive a more favorable label than our product candidates.

Intellectual Property

We actively seek to protect the intellectual property and proprietary technology production platform that we believe is important to our business, which includes seeking and maintaining patents covering our technology production platform and products, and any other inventions that are commercially or strategically important to the development of our business. We also seek to protect the confidentiality of trade secrets that may be important to the development of our business. Our ability to stop third parties from making, using, selling, offering to sell, or importing our products may depend on the extent to which we have rights under valid and enforceable patents or trade secrets that cover these activities. In addition, we believe our first-ever, wholly-owned, discovered in-house platform, which is capable of generating a diverse repertoire of multi-specific, targeted, fully human immunoglobulins (hIgG), is unique, and we leverage a multi-level IP strategy with no biosimilar pathway creating high barriers to entry.

For more information, please see “Risk Factors – Risks Related to Our Intellectual Property”.

The portfolio of intellectual property and trade secrets that we have developed includes patents related to the activity of our HAC and methods that we expect to generate hIgG at commercial scale. The patent portfolio includes composition and method patents. Our goal is to continue expansion of the breadth of claims and length of claim protections. Our technologies may be difficult to replicate, creating potential barriers to entry, as our genetic engineering know-how and suite of proprietary production platform IP and trade secrets have been developed and optimized over nearly two decades.

We expect our global patent protection to extend to 2041 and beyond with respect to producing commercial-scale hIgG using our chromosome engineering that generates high concentrations of hIgG in ungulates. However, we recognize that patents and other intellectual property rights in biotechnology are constantly evolving with many risks and uncertainties, which may affect those rights.

As of March 2026, our patent portfolio includes over 50 issued patents or pending applications. We have made strategic filings in jurisdictions including the United States, Australia, Canada, China, Europe, Japan, and Korea.

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These patent families cover:

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Granted patents in the U.S., Europe, Japan, and other major markets relating to a HAC vector comprising a gene encoding the human antibody heavy chain, a gene encoding the human antibody light chain, and and optionally a gene encoding IgM heavy chain constant region derived (at least in part) from an ungulate and an ungulate class switch regulatory element (expiring in 2033).

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Granted patents in the U.S., Europe, Japan, and other major markets relating to a HAC vector comprising a gene encoding the human antibody heavy chain, a gene encoding the human antibody light chain, and a gene encoding IgM heavy chain constant region derived (at least in part) from an ungulate (expiring in 2030 and in the U.S., 2031).

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Granted U.S. patents relating to methods for producing hIgG against a pathogen comprising injecting a non-human animal with a pathogen-derived DNA vaccine in at least two locations of the animal (expiring in 2036).

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Granted U.S. patent and a pending U.S. application covering ungulate-derived human immunoglobulins that specifically bind coronavirus S protein, and methods of making and using the same in treating or preventing coronavirus disease (expiring in 2041).

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Related to anti-thymocyte globulin (ATG) products, pending patent applications in the U.S., Europe, Japan, and other major markets covering ungulate-derived polyclonal immunoglobulin compositions comprising -human or substantially human immunoglobulins that specifically bind human thymocytes, T cells, B cells, and/or monocytes, and methods of making and using the same in treating or preventing organ transplant rejection or T1D (if issued, naturally expiring in 2041).

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Additionally related to anti-thymocyte globulin (ATG) products, pending PCT and U.S. patent applications covering ungulate-derived polyclonal immunoglobulin compositions comprising human or substantially human immunoglobulins that specifically bind human thymocytes, and improved methods of making and using the same in treating or preventing T1D (if issued, naturally expiring in 2045).

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Pending U.S. and European applications covering ungulate-derived hIgG that specifically bind influenza antigen, and methods of making and using the same in treating or preventing influenza (if issued, naturally expiring in 2042) and improvements thereof (if issued, naturally expiring in 2044).

US Patent System

In most countries in which we file patents, including the United States, the patent term is 20 years from the earliest date of filing a non-provisional patent application. In the United States, a patent’s term may potentially be lengthened by patent term adjustment, which compensates a patentee for administrative delays by the United States Patent and Trademark Office (the “US PTO”) in examining and granting a patent considering delays on the part of the patentee or may be shortened if a patent is terminally disclaimed over an earlier filed patent. In the United States, the patent term that covers an FDA-licensed biologic may also be eligible for patent term extension, which permits patent term restoration as compensation for the patent term lost during the FDA regulatory review process. The Hatch-Waxman Act permits a patent term extension of up to five years beyond the expiration of the patent. The length of the patent term extension is related to the length of time the drug is under regulatory review. Patent term extension cannot extend the remaining term of a patent beyond a total of 14 years from the date of product licensure, only one patent applicable to a licensed biologic may be extended and only those claims covering the licensed biologic, a method for using it, or a method for manufacturing it may be extended. Similar provisions are available in Europe and other foreign jurisdictions to extend the term of a patent that covers a licensed biologic. In the future, if and when our product candidates receive FDA approval or licensure, we expect to apply for patent term extensions on patents covering those products. We expect to seek patent term extensions to any of our issued patents in any jurisdiction where these are available, however there is no guarantee that the applicable authorities, including the FDA in the United States, will agree with our assessment of whether such extensions should be granted, and if granted, the length of such extensions. For more information regarding the risks related to our intellectual property, see the section titled “Risk Factors – Risks Related to Our Intellectual Property”.

US Patent Term Restoration

Depending upon the timing, duration, and specifics of FDA approval of product candidates, some of a sponsor’s U.S. patents may be eligible for limited patent term extension under the Drug Price Competition and Patent Term Restoration Act of 1984, or the Hatch-Waxman Amendments. The Hatch-Waxman Amendments permit a patent restoration term of up to five years as compensation for patent term lost during the product development and FDA regulatory review process. However, patent term restoration cannot extend the remaining term of a patent beyond a total of 14 years from the product’s approval or licensure date. The patent term restoration period generally is- once the patent issues- one-half the time between the effective date of an IND and the submission date of a biologics license application (“BLA”) less any time the sponsor did not act with due

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diligence during the period, plus the time between the submission date of a BLA and the approval of that application less any time the sponsor did not act with due diligence during the period. Only one patent applicable to an approved biological product is eligible for the extension, only those claims covering the licensed biologic, a method for using it or a method for manufacturing it may be extended and the application for the extension must be submitted prior to the expiration of the patent. Moreover, a given patent may only be extended once based on a single product. The U.S. PTO, in consultation with the FDA, reviews and approves the application for any patent term extension or restoration.

Government Regulations in the United States

In the United States, we expect our hIgG product candidates to be regulated by the FDA as biological products. Additionally, in manufacturing our product candidates, we alter the genomic DNA in animals, and FDA considers such altered genomic DNA in an animal to be a new animal drug, which require submission and approval of a New Animal Drug Application (NADA) prior to being marketed in the United States.

Regulation of Transgenic Animals and New Animal Drugs

The U.S. Department of Agriculture (the “USDA”) regulates the company’s Tc Bovine husbandry activities, including housing, healthcare, and general management of these specialized animals. This includes regulations and periodic facility inspections and reporting. We also are voluntarily accredited by the AAALAC. The AAALAC International accreditation program evaluates organizations that use animals in research, teaching or testing. Those that meet or exceed AAALAC standards are awarded accreditation. The accreditation process includes an extensive internal review conducted by the institution applying for accreditation.

The FDA considers, with limited exclusions, the altered genomic DNA in an animal to be a drug because such altered DNA is an article intended to affect the structure or function of the body of the animal, and, in some cases, intended for use in the diagnosis, cure, mitigation, treatment, or prevention of disease in the animal. In the United States, new animal drugs are subject to regulation under the Federal Food, Drug, and Cosmetic (FDCA), and under the FDCA, in general, a new animal drug is “deemed unsafe” and adulterated unless the FDA has approved a NADA for its intended use or unless the drug is only for investigational use and conforms to specified exemptions for such use under an investigational new animal drug (INAD) exemption. Further, early in the development process, FDA has allowed the submission of information to FDA’s Center for Veterinary Medicine (the “CVM”), without the establishment of an INAD file, such as through creation of a veterinary master file (VMF), subject to certain conditions such as restrictions on introducing any food derived from such investigational animals into the food supply.

The requirements governing development and approval of a new animal drug are analogous to those for new human drugs. A NADA must generally be accompanied by payment of a substantial user fee and must contain substantial evidence of the safety and effectiveness of the new animal drug as well as detailed descriptions of the methods used in and the facilities and controls used for the manufacturing, processing and packaging of the new animal drug to enable FDA to reach a determination that such methods, facilities and controls are adequate to preserve the identity, strength, quality and purity of the new animal drug. Further, when FDA reviews and approves a NADA, FDA generally conducts a review of environmental risks pursuant to the requirements of the National Environmental Policy Act (NEPA), if any and where required.

U.S. Biological Products Development Process

In the United States, biologic products are licensed by the FDA for marketing under the Public Health Service Act, (PHS Act), and regulated under the FDCA. Both the FDCA and the PHS Act and their corresponding regulations govern, among other things, the testing, manufacturing, safety, purity, potency, efficacy, labeling, packaging, record keeping, storage, distribution, marketing, sales, import, export, reporting, advertising, and other promotional practices involving biologic products. FDA authorization is required prior to clinical testing of biologic products. FDA licensure also must be obtained prior to marketing of biologic products. The process of obtaining regulatory approvals and the subsequent compliance with appropriate federal, state, local and foreign statutes and regulations require the expenditure of substantial financial resources and time.

Hybrid Process for a Biological Product is Developed from Animals with Intentionally Altered Genomic DNA

The process required by the FDA before a biologic product may be marketed in the United States is generally well documented. In the case of a product that is developed from animals with intentionally altered genomic DNA as the donor material source, the process is more complex and involves both CVM, to oversee the intentionally altered genomic DNA in animals and the Office of Tissues and Advanced Therapies (OTAT) at CBER to oversee the immunoglobulin products.

During all phases of clinical development, regulatory agencies require extensive monitoring and auditing of all clinical activities, clinical data, and clinical trial investigators. Annual progress reports detailing the results of the clinical trials must

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be submitted to the FDA. Written INAD and IND safety reports must be promptly submitted to the FDA and the investigators for serious and unexpected adverse events, any findings from other studies, tests in laboratory animals or in vitro testing that suggest a significant risk for human subjects, or any clinically important increase in the rate of a serious suspected adverse reaction over that listed in the protocol or investigator brochure. The sponsor must submit an IND safety report within 15 calendar days after the sponsor determines that the information qualifies for reporting. The sponsor also must notify the FDA of any unexpected fatal or life-threatening suspected adverse reaction within seven calendar days after the sponsor’s initial receipt of the information. Phase 1, Phase 2, and Phase 3 clinical trials may not be completed successfully within any specified period, if at all. The FDA or the sponsor or its data safety monitoring board may suspend a clinical trial at any time on various grounds, including a finding that the research subjects or patients are being exposed to an unacceptable health risk. Similarly, an IRB can suspend or terminate approval of a clinical trial at its institution if the clinical trial is not being conducted in accordance with the IRB’s requirements or if the biologic has been associated with unexpected serious harm to patients.

Concurrent with clinical trials, companies usually complete additional animal studies and must also develop additional information about the physical characteristics of the biologic as well as finalize a process for manufacturing the product in commercial quantities in accordance with GMP requirements. To help reduce the risk of the introduction of adventitious agents with the use of biologics, the PHS Act emphasizes the importance of manufacturing control for biologic products whose attributes cannot be precisely defined. The manufacturing process must be capable of consistently producing quality batches of the product candidate and, among other things, the sponsor must develop methods for testing the identity, strength, quality, potency, and purity of the final biological product. Additionally, appropriate packaging must be selected and tested, and stability studies must be conducted to demonstrate that the biological product candidate does not undergo unacceptable deterioration over its shelf life.

There are also various laws and regulations regarding laboratory practices, the experimental use of animals and the use and disposal of hazardous or potentially hazardous substances in connection with the research. In each of these areas, the FDA and other regulatory authorities have broad regulatory and enforcement powers, including the ability to levy fines and civil penalties, suspend or delay issuance of approvals, seize or recall products and withdraw approvals.

U.S. Review and Approval Processes

Assuming successful completion of all required testing in accordance with all applicable regulatory requirements, the results of product development, nonclinical studies and clinical trials are submitted to the FDA as part of a NADA requesting approval of the altered genomic DNA in donor animals and a BLA requesting approval to market the product for one or more indications. The BLA must include results of product development, laboratory and animal studies, human studies, information on the manufacture and composition of the product, proposed labeling, and other relevant information. The testing and approval processes require substantial time and effort, and there can be no assurance that the FDA will accept the BLA for filing and, even if filed, that any approval will be granted on a timely basis, if at all.

Under the Prescription Drug User Fee Act (PDUFA), as amended, each BLA may be accompanied by a significant user fee. Under federal law, the submission of most applications for approval of drug and biologic products is subject to an application user fee. The sponsor of an approved application is also subject to an annual program fee. Fee waivers or reductions are available in certain circumstances, including a waiver of the application fee for the first application filed by a small business.

Within 60 days following submission of a BLA or within 30 days following submission of a NADA, the FDA reviews the submitted application to determine if it is substantially complete before the FDA accepts it for filing. The FDA may refuse to file any application that it deems incomplete or not properly reviewable at the time of submission and may request additional information. In this event, the application must be resubmitted with additional information. The resubmitted application also is subject to review to determine if it is substantially complete before the FDA accepts it for filing. In most cases, the submission of an application to FDA is subject to a substantial application user fee, although the fee may be waived under certain circumstances.

Under the performance goals and policies implemented by the FDA under the Animal Drug User Fee Act (ADUFA) for original NADAs, the FDA targets 180 days from the submission date in which to complete its initial review and act on a standard application. A NADA is considered incomplete if it requires additional data or information to enable the FDA to complete and reach a decision on issues presented in the NADA. Once the sponsor reactivates the NADA by addressing identified deficiencies, the FDA targets 135 to 180 days, depending in part on whether the deficiencies are identified as not substantial or substantial, respectively, to complete its review and respond to the applicant.

The sponsor of a new animal drug may voluntarily decide to utilize FDA’s “phased review” process to complete all technical sections required for approval of a new animal drug before submitting a NADA by submitting such information during the investigational phase of the animal drug development process. Utilizing this process, the sponsor may submit an administrative NADA, which is a NADA submitted after all technical sections necessary to fulfill the requirements for the

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approval of a new animal drug have been reviewed by the CVM and the CVM has issued a technical section complete letter for each of the required technical sections. The FDA targets 60 days from the filing date to complete its review and act on an administrative NADA.

Under the performance goals and policies implemented by the FDA under the PDUFA for original BLAs, the FDA targets ten months from the filing date in which to complete its initial review of a standard application and respond to the applicant, and six months from the filing date for an application with priority review. The FDA does not always meet its PDUFA goal dates, and the review process is often significantly extended by FDA requests for additional information or clarification.

Once the submission is accepted for filing, the FDA begins an in-depth substantive review of the NADA and BLA. The FDA reviews the applications to determine, among other things, whether the proposed product is safe, pure, and potent, for its intended use, and whether the product is being manufactured in accordance with cGMP to ensure its continued safety, purity, and potency. The FDA may refer applications for novel biological products or biological products that present difficult or novel questions of safety or efficacy to an advisory committee, typically a panel that includes clinicians and other experts, for review, evaluation, and a recommendation as to whether the application should be approved and under what conditions. The FDA is not bound by the recommendations of an advisory committee, but it considers such recommendations carefully when making decisions. During the biological product approval process, the FDA also will determine whether a REMS is necessary to assure the safe use of the biological product. If the FDA concludes a REMS is needed, the sponsor of the BLA must submit a proposed REMS; the FDA will not approve the BLA without a REMS, if required.

Post-Approval Requirements

Maintaining substantial compliance with applicable federal, state, and local statutes and regulations requires the expenditure of substantial time and financial resources. Rigorous and extensive FDA regulation of biological products continues after approval, particularly with respect to GMP. We will rely, and expect to continue to rely, on third parties to produce clinical and commercial quantities of any products that we may commercialize. Manufacturers of our products are required to comply with applicable requirements in the GMP regulations, including quality control and quality assurance and maintenance of records and documentation.

Following approval, the manufacturing facilities are subject to periodic inspections by the FDA, and such inspections may result in an issuance of FDA Form 483 deficiency observations, an untitled letter, or a warning letter, which can lead to plant shutdown and other more serious penalties and fines. Prior to the institution of any manufacturing changes, a determination needs to be made whether FDA approval is required in advance. If not done in accordance with FDA expectations, the FDA may restrict supply and may take further enforcement action. Annual product reports are required to be submitted. Other post-approval requirements applicable to biological products include reporting of GMP deviations that may affect the identity, potency, purity and overall safety of a distributed product, record-keeping requirements, reporting of adverse events, reporting updated safety and efficacy information, and complying with electronic record and signature requirements.

Additionally, rigorous and extensive FDA regulation of new animal drugs continues after approval. Owners of approved NADAs continue to have ongoing responsibilities under the FDCA, including registration and listing, recordkeeping, filing supplements, and periodic reporting.

Expedited Review and Approval Programs

The FDA has various programs, including fast track designation, priority review, accelerated approval and breakthrough therapy designation, which are intended to expedite or simplify the process for the development and FDA review of biological products that are intended for the treatment of serious or life-threatening diseases or conditions and demonstrate the potential to address unmet medical needs. The purpose of these programs is to provide important new biological products to patients earlier than under standard FDA review procedures. To be eligible for a fast-track designation, the FDA must determine, based on the request of a sponsor, that a biological product is intended to treat a serious or life-threatening disease or condition and demonstrates the potential to address an unmet medical need. The FDA will determine that a product will fill an unmet medical need if it will provide a therapy where none exists or provide a therapy that may be potentially superior to existing therapy based on efficacy or safety factors. In addition to other benefits, such as the ability to have greater interactions with the FDA, the FDA may initiate review of sections of a fast track BLA before the application is complete, a process known as rolling review.

The FDA may give a priority review designation, such as a rare pediatric disease designation, to biological products that treat a serious condition and, if approved, would provide a significant improvement in safety or effectiveness. A priority review means that the goal for the FDA’s review of an application is six months, rather than the standard goal of ten months under current PDUFA guidelines. Most products that are eligible for fast-track designation may also be considered appropriate to receive a priority review. In addition, biological products studied for their safety and effectiveness in treating serious or life-threatening illnesses and that provide meaningful therapeutic benefit over existing treatments may receive accelerated

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approval and may be approved on the basis of adequate and well-controlled clinical trials establishing that the biological product has an effect on a surrogate endpoint that is reasonably likely to predict clinical benefit, or on a clinical endpoint that can be measured earlier than irreversible morbidity or mortality, that is reasonably likely to predict an effect on irreversible morbidity or mortality or other clinical benefit, taking into account the severity, rarity or prevalence of the condition and the availability or lack of alternative treatments.

Under the FDA Safety and Innovation Act enacted in 2012, a sponsor can request designation of a product candidate as a “breakthrough therapy.” A breakthrough therapy is defined as a drug or biological product that is intended, alone or in combination with one or more other drugs or biologics, to treat a serious or life-threatening disease or condition and preliminary clinical evidence indicates that the drug or biological product may demonstrate substantial improvement over existing therapies on one or more clinically significant endpoints, such as substantial treatment effects observed early in clinical development. Breakthrough therapy designation comes with all the benefits of fast-track designation, which means that the sponsor may file sections of the BLA for review on a rolling basis if certain conditions are satisfied, including an agreement with the FDA on the proposed schedule for submission of portions of the application and the payment of applicable user fees before the FDA may initiate a review. Drug and biological products designated as breakthrough therapies are also eligible for accelerated approval. The FDA must take certain actions, such as holding timely meetings and providing advice, intended to expedite the development and review of an application for approval of a breakthrough therapy.

Even if a product qualifies for one or more of these programs, the FDA may later decide that the product no longer meets the conditions for qualification and the time period for FDA review or approval will not be shortened. Furthermore, fast track designation, priority review, accelerated approval and breakthrough therapy designation do not change the standards for approval and may not ultimately expedite the development or approval process.

Orphan Drug Designation

Under the Orphan Drug Act, the FDA may grant orphan designation to a drug or biologic intended to treat a rare disease or condition, which is a disease or condition that affects fewer than 200,000 individuals in the United States, or 200,000 or more individuals in the United States for which there is no reasonable expectation that the cost of developing and making available in the United States a drug or biologic for this type of disease or condition will be recovered from sales in the United States for that drug or biologic. Orphan drug designation must be requested before submitting a BLA. After the FDA grants orphan drug designation, the generic identity of the therapeutic agent and its potential orphan use are disclosed publicly by the FDA. The orphan drug designation does not convey any advantage in, or shorten the duration of, the regulatory review or approval process.

Pediatric Trials

Under the Pediatric Research Equity Act (PREA), a BLA or supplement to a BLA must contain data to assess the safety and efficacy of the product for the claimed indications in all relevant pediatric subpopulations and to support dosing and administration for each pediatric subpopulation for which the product is safe and effective. The FDCA requires that a sponsor who is planning to submit a marketing application for a drug or biologic product that includes a new active ingredient, new indication, new dosage form, new dosing regimen or new route of administration submit an initial Pediatric Study Plan, or PSP, within sixty days of an end-of-Phase 2 meeting or as may be agreed between the sponsor and FDA. The initial PSP must include an outline of the pediatric study or studies that the sponsor plans to conduct, including study objectives and design, age groups, relevant endpoints and statistical approach, or a justification for not including such detailed information, and any request for a deferral of pediatric assessments or a full or partial waiver of the requirement to provide data from pediatric studies along with supporting information. The FDA and the sponsor must reach agreement on the PSP. A sponsor can submit amendments to an agreed-upon initial PSP at any time if changes to the pediatric plan need to be considered based on data collected from nonclinical studies, early phase clinical trials, and/or other clinical development programs. The FDA may, on its own initiative or at the request of the applicant, grant deferrals for submission of some or all pediatric data until after approval of the product for use in adults, or full or partial waivers from the pediatric data requirements.

Marketing Exclusivity

Depending upon the timing, duration, and specifics of the FDA approval of the use of our product candidates, some of our United States patents may be eligible for limited patent term extension under the Hatch-Waxman Amendments. The Hatch-Waxman Amendments permit a patent restoration term of up to five years as compensation for patent term lost during product development and the FDA regulatory review process. However, patent term restoration cannot extend the remaining term of a patent beyond a total of 14 years from the product’s approval date. The patent term restoration period is generally one-half the time between the effective date of an IND and the submission date of a BLA plus the time between the submission date of a BLA and the approval of that application. Only one patent applicable to an approved biological product is eligible for the extension and the application for the extension must be submitted prior to the expiration of the patent. In

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addition, a patent can only be extended once and only for a single product. The U.S. PTO, in consultation with the FDA, reviews and approves the application for any patent term extension or restoration. The Biologics Price Competition and Innovation Act of 2009 (“BPCIA”), which was enacted as part of the Patient Protection and Affordable Care Act of 2010, as amended by the Health Care and Education Reconciliation Act of 2010 (the “ACA”), created an abbreviated approval pathway for biological products that are demonstrated to be “biosimilar” or “interchangeable” with an FDA-licensed reference biological product via an approved BLA. Biosimilarity to an approved reference product requires that there be no differences in conditions of use, route of administration, dosage form and strength and no clinically meaningful differences between the biological product and the reference product in terms of safety, purity, and potency. Biosimilarity is demonstrated in steps beginning with rigorous analytical studies or “fingerprinting,” in vitro studies, in vivo animal studies and generally at least one clinical study, absent a waiver from the Secretary of the U.S. Department of Health and Human Services (“HHS”). As previously mentioned, there is no biosimilar pathway for the complexity that exists in a polyclonal antibody drug product.

Additional Regulation

In addition to the foregoing, state and federal laws regarding environmental protection and hazardous substances, including the Occupational Safety and Health Act, the Resource Conservancy and Recovery Act and the Toxic Substances Control Act, affect our business. These and other laws govern our use, handling and disposal of various biological, chemical, and radioactive substances used in, and wastes generated by, our operations. If our operations result in contamination of the environment or expose individuals to hazardous substances, we could be liable for damages and governmental fines. We believe that we are in material compliance with applicable environmental laws and that continued compliance therewith will not have a material adverse effect on our business. We cannot predict, however, how changes in these laws may affect our future operations.

Government Regulation Outside of the United States

In addition to regulations in the United States, we are, and will continue to be, subject to a variety of regulations in other jurisdictions governing, among other things, clinical studies and any commercial sales and distribution of our products. Because biologically sourced raw materials are subject to unique contamination risks, their use may be restricted in some countries. Whether or not we obtain FDA approval for a product, we must obtain the requisite approvals from regulatory authorities in foreign countries prior to the commencement of clinical studies or marketing of the product in those countries. Certain countries outside of the United States have a similar process that requires the submission of a clinical study application much like the IND prior to the commencement of human clinical studies.

If we fail to comply with applicable foreign regulatory requirements, we may be subject to, among other things, fines, suspension or withdrawal of regulatory approvals, product recalls, seizure of products, operating restrictions, and criminal prosecution.

Our Corporate History

SAB Sciences, Inc. (formerly SAB Biotherapeutics, Inc.) was incorporated in April 2014 as a Delaware corporation (“Legacy SAB”). We acquired all the intellectual property rights to Tc Bovine and the production platform from Sanford Applied Biosciences, a wholly owned subsidiary of Sanford Health, to develop targeted hIgG to specific targets and advance clinical development and commercialization. The technology was originally contemplated in 1998 by professors at the University of Massachusetts Amherst and Amherst College who recognized a significant gap in immunotherapy applications, namely, using the way our bodies fight disease through a hIgG response. The technology founders established a biotech company called “Hematech” to develop the technology. This founding company was purchased and became a wholly owned subsidiary of Kirin in Tokyo, Japan in 2005. In 2007, the pharmaceutical division of Kirin became Kirin Pharma and in 2008 merged with Kyowa Hakko Kogyo to become Kyowa Hakko Kirin (“KHK”). The technology was developed through 2012 by Hematech as a wholly owned subsidiary of KHK. On December 31, 2012, KHK divested the technology and transferred ownership of all property, assets, and intellectual property of Hematech to Sanford Health and the technology was further developed by Sanford Applied Biosciences until we acquired it in its entirety in June 2014.

Since acquiring the technology in 2014, we have continued to develop intellectual property and specifically targeted hIgG to multiple disease indications, and we have conducted or collaborated in eight clinical trials (six of which are in review), where we have demonstrated safety and efficacy in multiple Tc Bovine-derived hIgG product candidates. We have developed our rapid response capabilities and completed proof of concept using private resources as well as over $200 million of funds awarded from the U.S. Government emerging disease and medical countermeasures programs.

In October 2021, we completed our business combination with Big Cypress Acquisition Corp. (“BCYP”), pursuant to which we debuted as a publicly traded company (the “Business Combination”). BCYP was incorporated as a special purpose

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acquisition company in the State of Delaware on November 12, 2020. On January 14, 2021, BCYP completed its initial public offering. On October 22, 2021, BCYP consummated the Business Combination with Legacy SAB, which changed its name from SAB Biotherapeutics, Inc. to Legacy SAB. In connection with the closing of the Business Combination, BCYP changed its name to SAB Biotherapeutics, Inc. and Legacy SAB became a wholly-owned subsidiary of SAB Biotherapeutics, Inc.

In June 2024, we announced a new brand, logo mark, and visual identity to reflect the company’s strategic evolution in immunotherapy as SAB BIO.

Available Information

Our principal executive offices are located at 777 W 41st St. Suite 401 Miami Beach, FL 33140, and our telephone number is (605)-679-6980. Our corporate website address is www.sab.bio. Our Annual Reports on Form 10-K, quarterly reports on Form 10-Q, current reports on Form 8-K and proxy statements, and all amendments thereto, are available free of charge on our website. These reports are posted on our website as soon as reasonably practicable after they are electronically filed with the U.S. Securities and Exchange Commission (the “SEC”). The public may read and copy any materials that we file with the SEC electronically through the SEC website (www.sec.gov). The information contained on the SEC’s website is not incorporated by reference into this Annual Report and should not be considered to be part thereof.

Human Capital

As of December 31, 2025, we had 86 full-time employees, and of these employees, 53 were engaged in research and development activities, 17 were engaged in clinical activities and 16 were engaged in general and administrative activities. As of December 31, 2025, none of our employees were represented by labor unions or covered by collective bargaining agreements. We consider our relationship with our employees to be good. We emphasize several measures and objectives in managing its human capital assets, including, among others, (i) employee safety and wellness, (ii) talent acquisition and retention, (iii) employee engagement, development, and training, (iv) diversity and inclusion and (v) compensation. These targeted ideals may include annual bonuses, stock-based compensation awards, a 401(k) plan with employee matching opportunities, healthcare, and insurance benefits, health savings and flexible spending accounts, paid time off, family leave, family care resources, and/or employee assistance programs. We also provide our employees with access to various innovative, flexible, and convenient health and wellness programs. We designed these programs to support employees’ physical and mental health by providing tools and resources to improve or maintain their health status and encourage engagement in healthy behaviors.