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Item 1. Business

2026-03-09 compared with 2025-03-31 · 210 added, 91 removed, 312 unchanged (49% of the section changed)

Business Overview

We are a clinical-stage biopharmaceutical company focused on the development of human polyclonal immunotherapeutic antibodies, or human immunoglobulin G (hIgG), to address immunology disorders.

We are a clinical-stage biopharmaceutical company focused on developing multi-specific, high-potency, human immunoglobulin G (hIgG) to treat and prevent immune and autoimmune disorders.

Our programs are based on mechanisms of action that have achieved proof-of-concept in clinical trials in indications with significant unmet medical needs.

We are focused on developing product candidates for disease targets where a differentiated approach has the greatest potential to be either first-in-class against novel targets or best-in-class against complex targets to treat diseases, including type 1 diabetes (T1D) and other autoimmune disorders.

Our internally discovered antibodies are both target-specific and polyclonal, meaning they are comprised of multiple hIgG and can bind to multiple sites on targeted immunogens, making them ideally suited to address the complexities associated with many immune-mediated disorders.

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.

We believe it is the only technology capable of producing disease-targeted, hIgG in large quantities without the need for human plasma donors.

We have optimized genetic engineering in the development of transchromosomic cattle, or Tc Bovine, which produce hIgG.

The Company’s lead candidate, SAB-142, targets autoimmune T1D with a disease-modifying therapeutic approach that aims to potentially change the T1D treatment paradigm by delaying onset and potentially preventing disease progression of Stage 3 T1D patients.

Using advanced genetic engineering and antibody science, we developed a proprietary technology which holds the potential to generate additional novel therapeutic candidates utilizing the human immune response, without the need for human donors or convalescent plasma.

We believe it is the only technology capable of producing disease-targeted, hIgG in large quantities without human plasma donors.

We have optimized genetic engineering in the development of transchromosomic cattle, or Tc-Bovine, to produce hIgG.

Our engineering of our production platform drives IgG1 production across our pipeline.

In addition, this differentiated approach using polyclonal antibodies has no biosimilar pathway, which provides a significant barrier to competitive polyclonal approaches.

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:

Our Lead Product Candidate

Our wholly owned lead product candidate, SAB-142 is a human anti-thymocyte globulin (ATG) focused on preventing or delaying the progression of T1D.

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.

SAB-142 is expected to reduce autoimmune β-cell destruction and delay progression or onset of T1D in patients with Stage 3 or Stage 2 T1D, respectively.

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

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).

addition, data from more than 700 human subjects treated with antibodies produced by our platform support expectation of a zero-serum sickness rate and zero incidence of neutralizing anti-drug antibodies (ADA) within the upcoming SAB-142 clinical trials.

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) as well as United Kingdom Medicines and Healthcare products Regulatory Agency (MHRA) and 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 CBER.

CBER has approved over 36 immunoglobulin products from both human- and animal-derived plasma.

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.

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As our lead program SAB-142 advances, we intend to expand our pipeline in complementary indications through strategic utilization of our platform.

We recently 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.

Next, we intend to advance SAB-142 into a Phase 2b clinical trial called the SAFEGUARD study which is anticipated to initiate mid-year 2025.

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

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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 is approved in the U.S.

only for patients with Stage 2 T1D and has been filed for approval in Europe for patients with Stage 3 T1D.

In addition, the treatment burden for Tzield for Stage 2 and Stage 3 T1D is one course of intravenous (IV) daily therapy for 12 days at Month 1 and two courses of IV daily therapy for 12 days, at Month 1 and Month 6, respectively.

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.

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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) administered intravenously over two days in an ambulatory setting, have shown statistically significant maintenance of C-peptide levels and thus a delay in progression of recent onset T1D.

Based on the results of a Phase 2 clinical trial 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.

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 subject 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 reduces the capacity to re-dose rATG when C-peptide levels begin to drop.

The below graph shows the statistically significant preservation of C-peptide (p=0.00005) over two years in low dose rATG.

The following table highlights the C-peptide response of anti-thymocyte globulin:

Low-Dose ATG* Preserved C-Peptide in New Onset T1D

In addition to the C-peptide data, rATG treated patients showed a significant reduction in glycated hemoglobin A1C (HbA1C) over the placebo group (p=0.002).

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.

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:

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.

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.

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

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.

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;

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.

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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 defined as a Type 3 hypersensitivity reaction.

Serum sickness is

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.

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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.

Our 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 re-dosing while eliminating the treatment burden observed with currently available therapies.

While the MoA of our compound closely resembles rATG, SAB-142 has clear advantages that are fundamental for safe and reliable re-dosing required to delay disease progression.

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.

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 sparing T regulatory (Treg) cells in addition to modulating other autoimmune pathways involved in T1D pathophysiology.

By reducing overreactive CD4+ and CD8+ T cells while preserving T reg cells, SAB-142 is expected to reduce autoimmune β-cell destruction and delay progression or onset of T1D in patients with Stage 3 or Stage 2 T1D respectively.

In addition to potentially preserving beta cell function in early T1D patients, SAB-142 offers the potential of safe and reliable re-dosing 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-142-101, SAB-142 demonstrated zero serum sickness and zero immunogenicity at the target dose levels, thus supporting its potential for safe and reliable redosing.

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.

The average age of clinical onset of T1D is 13 years old.

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.

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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 re-dosing potentially aimed at fully preventing clinical onset of disease.

The ultimate vision for SAB-142 is founded on the potential ability to safely re-dose by delivering a consistent and effective dose of this medication only once per year to fully halt progression of established clinical disease or delay its onset indefinitely.

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 plan to advance SAB-142 into a Phase 2b trial in 2025 to evaluate the therapeutic candidate in adult and pediatric patients with new-onset T1D.

The SAB-142 Phase 1 clinical trial was designed as a randomized, double-blind, placebo-controlled, single-ascending dose, adaptive design clinical study among healthy volunteers and one cohort of participants with T1D that commenced dosing in November 2023.

The objectives include establishing the safety, tolerability, pharmacokinetic (PK), immunogenicity and pharmacodynamic (PD) profile for SAB-142.

The reported topline results showed the following outcomes among healthy volunteer cohorts:

Based on the data, we advanced SAB-142 into a registrational Phase 2b trial, SAF ety and E fficacy of human anti-thymocyte immuno G lob U lin SAB-142 AR resting progression of type 1 D iabetes (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 HU man 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:

• Favorable safety profile:

SAB-142 was generally well-tolerated and demonstrated a favorable safety profile that supports the chronic dosing of SAB-142 in an ambulatory setting.

The SAB-142 Phase 1 dose range was between 0.03mg/kg up to 2.5mg/kg, which demonstrated favorable safety profile based on the 0% reported serum sickness and ADAs.

• Sustained Immunomodulation:

SAB-142 demonstrated a clinically validated multi-target MOA with sustained immunomodulation.

• Mechanism of Action Analogous to Rabbit ATG:

The MOA of SAB-142 was shown to be analogous to rabbit ATG.

The SAB-142 MOA was shown to be analogous to rabbit ATG across multiple parameters correlative to C-peptide preservation.

Based on the completed Phase 1 clinical trial, we plan on initiating a global Phase 2b study, SAFEGUARD ( SAF ety and E fficacy of human anti-thymocyte immuno G lob U lin SAB-142 AR resting progression of type 1 D iabetes), which would be a randomized, double blinded, placebo controlled, dose ranging study in new onset pediatric, adolescent and adult Stage 3 T1D patients.

The primary endpoint is stimulated C-peptide following a 2-hour mixed meal tolerance test (MMTT) at 12 months and secondary endpoints are time in range, time in tight Range, time below range, prandial insulin use, HbA1c, hypoglycemic episodes and safety.

This Phase 2b study is expected to initiate in the middle of 2025 with interim data in the middle of 2026 and topline data in 2027.

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

infusion-site reactions including pruritus and tenderness.

The most common AE was headache, which is consistent with typical AEs for T-cell modifying therapies.

• 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.

o 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

combined 1.5 mg/kg and 2.5 mg/kg dosed cohorts.

o 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

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

combined 1.5 mg/kg and 2.5 mg/kg dosed cohorts.

o 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.

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

combined 1.5 mg/kg and 2.5 mg/kg dosed cohorts.

• 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.

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.

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.

• 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%;

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.

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

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.

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.

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 variety of autoimmune diseases and our in vivo and in vitro pre-clinical and Phase 1 work from SAB-142 in T1D will support direct progression into Phase 2 clinical trials in other autoimmune indications.

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

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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 represent a “plug-and-play” approach:

The discovery, development, and production process represents a “plug-and-play” approach:

• Develop Immunogen for Disease Target .

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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.

In addition, we maintain supportive laboratory facilities and operations in Sioux Falls, South Dakota, for drug discovery, product and process development, and clinical manufacturing.

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

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.

We recently completed an expansion of our research and development laboratory facilities to accommodate our discovery programs, support for our pre-clinical pipeline programs, and process development research for our clinical product candidates.

The upstream process is easily scalable.

Animals donate plasma three times per month (2.1% of bodyweight each time).

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.

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, IM Therapeutics, Sernova, and Biomea Fusion.

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.

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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, our differentiated approach using polyclonal antibodies has no biosimilar pathway which provides a significant barrier to competitive polyclonal approaches.

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”.

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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, Korea, and Mexico.

We have made strategic filings in jurisdictions including the United States, Australia, Canada, China, Europe, Japan, and Korea.

These patent families cover:

• 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 a nonhuman animal (expiring in 2033).

• Granted patents in the U.S., Europe, Japan, and other major markets relating to large-scale production of hIgG by transgenic animals with high production of hIgG of at least 1 g/L in sera (expiring in 2030 and in the U.S., 2031).

• A granted U.S.

patent and a pending U.S.

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

• 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).

• Granted U.S.

patent 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).

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).

• 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).

• 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).

• 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).

• Pending U.S.

provisional application 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).

• A granted U.S.

patent relating to reprogramming a call to express a T-cell receptor reactive with an antigen of interest (expiring in 2025).

This patent is not material to the Company at this time, and we believe patents issued subsequently allow the Company to maintain its competitive position.

• Granted U.S.

patents covering cloned transgenic ungulates (e.g., bovines) in which prion protein activity is reduced by one or more genetically engineered mutations (expiring in 2025).

These patents are not material to the Company at this time, and we believe patents issued subsequently allow the Company to maintain its competitive position.

• Granted U.S.

patent relating to methods of cloning a non-human mammal using transgenic ungulate embryos of one or more cells that have a human chromosome fragment and transgenic ungulate embryos of one or more cells that have a human chromosome fragment, and methods for making them (expired in March 2025).

These patents

are not material to the Company, and we believe patents issued subsequently allow the Company to maintain its competitive position.

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

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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 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.

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.

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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.

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 (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.

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 identify, strength, quality and purity of the new animal drug.

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.

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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 be submitted to the FDA.

Annual progress reports detailing the results of the clinical trials must

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.

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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 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.

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

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.

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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 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.

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.

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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.

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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 addition, a patent can only be extended once and only for a single product.

addition, a patent can only be extended once and only for a single product.

PTO, in consultation with the FDA, reviews and approves the application for any patent term extension or restoration.

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We cannot predict, however, how changes in these laws may affect our future operations.

Government Regulation - Regulation Outside of the United States

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.

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(“BCYP”), pursuant to which we debuted as a publicly traded company (the “Business Combination”).

BCYP was incorporated as a special purpose acquisition company in the State of Delaware on November 12, 2020.

BCYP was incorporated as a special purpose

acquisition company in the State of Delaware on November 12, 2020.

On January 14, 2021, BCYP completed its initial public offering.

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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.

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.

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.

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Compared sentence by sentence after normalising whitespace, quotation marks, case and digits, so re-formatting and restated figures do not read as changed language. Wording changes appear as one removal and one addition. The current filing and the prior one are authoritative.

What changed 10-K

Item 1. Business