How SAB-142 works

The science behind SAB-142

Scientist in a white lab coat taking notes on a clipboard while talking with a colleague

SAB-142 is an investigational, fully human antibody therapy in clinical development for autoimmune type 1 diabetes (T1D).

It is designed to reduce the overreactive immune response and preserve beta cells that produce insulin with the goal of delaying disease progression in T1D.

Smiling woman sitting on a park bench with a coffee cup, wearing a sensor patch on her upper arm

How T1D is treated today



Type 1 diabetes is an autoimmune disease, driven by overreactive T cells that attack insulin-producing beta cells in the pancreas. In the US, approximately 2 million people have insulin-dependent, symptomatic T1D with roughly 64,000 newly diagnosed each year.1,2 For decades, the standard of care has been insulin replacement. However, that approach does not address the underlying autoimmune attack, which means the destruction of beta cells continues.

As beta cells are destroyed, the body loses its ability to produce endogenous insulin (insulin naturally produced by the body), increasing the risk of poor glycemic control and associated comorbidities.

We are taking a new approach: developing a disease-modifying therapy to modulate the immune system in order to help preserve insulin-producing beta cells.

A validated mechanism, with fully human antibodies

Studies with low dose of rabbit-derived ATG (rATG) have shown that this approach can help preserve the body’s remaining insulin-producing cells and improve blood sugar control in people with newly diagnosed and established Stage 3 T1D.3-5

Illustration of a SAB-142 antibody

Multispecific.
Fully human.

SAB-142 is a multispecific, fully human anti-thymocyte immunoglobulin (hATG) designed to target multiple immune cells involved in the destruction of insulin-producing beta cells.

No serum sickness and low immunogenicity due to fully human source, supporting potential for safe redosing.

Illustration of SAB-142 antibodies attaching to a T cell

Exhausting the “bad acting” T-cells driving the autoimmune attack

SAB-142 is designed to promote T-cell exhaustion without lymphodepletion or broad immunosuppression.

T-cell exhaustion has been linked to C-peptide preservation.3,4,6 C-peptide is a well-established biomarker of insulin production by pancreatic beta cells.

Illustration of a regulatory T cell (Treg) protected inside a shield

Preserving and activating Tregs to support immune self-tolerance

Regulatory T cells (Tregs) help control overreactive immune cells and maintain self-tolerance. SAB-142 is designed to preserve Tregs, allowing them to reduce the autoimmune hyperactivity, potentially helping rebalance the immune response and protect insulin-producing beta cells.

Tregs are the “peacekeepers” maintaining balance in the immune system.

Patient reading a magazine in a chair while receiving an IV infusion

Designed for long-term use

T1D is a chronic autoimmune disease requiring long-term management. In the Phase 1 study, SAB-142 was generally well tolerated and demonstrated a favorable safety profile, with no serum sickness and low immunogenicity. As a fully human biologic, SAB-142 is designed to overcome key limitations of non-human approaches and has the potential to enable long-term, repeat dosing to delay progression of T1D.

In the clinical study, SAB-142 is administered as a 
2-day infusion course, repeated every 6 months. The potential for redosing over the long term is a potential therapeutic advantage.

Two women smiling and talking over mugs at a kitchen table

Evaluating SAB-142 across a broad patient population

While many T1D clinical studies focus on the first 100 days following Stage 3 diagnosis, a significant unmet need remains for people beyond this window who still have residual beta cell function. SAB-142 is being studied in the investigator-led Phase 3 PRISE-hATG study, enrolling people aged 5 to 40 years who are 100 days to 2 years following a Stage 3 T1D diagnosis. The study is assessing the safety, efficacy, and tolerability of SAB-142, expanding the opportunity to evaluate disease modification up to 2 years after Stage 3 T1D onset and offering new hope to patients outside the newly diagnosed window.

Find out more about SAFEGUARD

See recent
publications

PRISE-hATG=Personalized Response and Immunologic Surveillance of Endogenous C-Peptide Preservation in New, Recent, and Extended New Onset T1D Treated with human Anti-Thymocyte Globulin.
SAFEGUARD=SAFety and Efficacy of Human Anti-thymocyte ImmunoGlobUlin SAB-142 ARresting Progression of Type 1 Diabetes.

References: 1. Rogers MAM, Kim C, Banerjee T, Lee JM. Fluctuations in the incidence of type 1 diabetes in the United States from 2001 to 2015: a longitudinal study. BMC Med. 2017;15(1):199. doi:10.1186/s12916-017-0958-6 2. Centers for Disease Control and Prevention. National Diabetes Statistics Report. Updated March 11, 2026. Accessed September 10, 2026. https://usdss.cdc.gov/diabetes/report.html 3. Haller MJ, Long SA, Blanchfield JL, 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. 2019;68(6):1267-1276. doi:10.2337/db19-0057 4. Mathieu C, Wych J, Hendriks AEJ, 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. Lancet. 2025;406(10510):1375-1388. doi:10.1016/S0140-6736(25)01674-5. 5. Haller MJ, Gitelman SE, Gottlieb PA, et al. Anti-thymocyte globulin/G-CSF treatment preserves β cell function in patients with established type 1 diabetes. J Clin Invest. 2015;125(1):448-455. doi:10.1172/JCI78492 6. Jacobsen LM, Diggins K, Blanchfield L, et al. Responders to low-dose ATG induce CD4+ T cell exhaustion in type 1 diabetes. JCI Insight. 2023;8(16):e161812. Published 2023 Aug 22. doi:10.1172/jci.insight.161812