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type1.science

End goal 02 — a cure

Road to a cure

From injected insulin to restoring the body's own insulin production — found early, protected, and durable.

This roadmap is the site’s spine: where we are today, the gaps stopping us, the research that would close them, and the questions still open. Every item and trial links back to the gap it advances.

  1. Stopping the immune attack

    T1D happens because the immune system destroys the body's own insulin-producing cells. Any durable cure has to stop or retrain that attack — otherwise new or replacement cells get destroyed too.

    Editorial estimate of progress35%

    Where we are today

    One therapy (teplizumab) can delay clinical onset by years in at-risk people — proof the attack can be slowed — and in 2026 the US widened that indication down to age 1. In June 2026 the FDA also granted accelerated approval for children aged 8–17 already diagnosed at stage 3, to slow the loss of the insulin production they have left: the first disease-modifying therapy approved for the newly diagnosed. It is still a brake, not a stop; it did not improve day-to-day glucose control; and continued approval depends on a confirmatory trial. Antigen-specific approaches that retrain immunity without blanket suppression remain unproven in people.

    What would close it

    • Antigen-specific immunotherapy that disarms only the T1D attack, sparing the rest of the immune system
    • Regulatory T-cell (Treg) therapies that re-establish tolerance
    • Combination immunotherapy timed to disease stage
    • Biomarkers that predict who responds, so treatment is targeted

    Open questions

    • Can the attack be stopped durably, not just delayed — and without lifelong immunosuppression?
    • Why do only some people respond to immune therapies, and can we tell in advance?
    • How early must you intervene — and now that treating at stage 3 preserves insulin production without improving day-to-day control, what does "enough to matter" actually mean for the person?
    Read the full picture →

    T1D is, at root, a case of mistaken identity: the immune system tags the body's own insulin-producing cells as a threat and destroys them.1 That is why insulin replacement is a treatment, not a cure — and why simply adding new cells isn't enough on its own. Drop fresh insulin-producing cells into an unchanged immune environment and the same attack picks up where it left off.

    The first real proof that the attack is bendable arrived with teplizumab, an anti-CD3 immune therapy. In a randomized trial of at-risk relatives, a single 14-day course pushed the median time to clinical diagnosis from about 24 months on placebo to about 48 months2 — and in extended follow-up the gap widened to roughly 60 versus 27 months, with measurable preservation of beta-cell function.3 That buys years and shows the disease clock isn't fixed. But a delay is not a stop, and broad immune-modulating drugs carry their own costs.

    Two US decisions in 2026 widened the window. In April, the FDA approved a supplemental filing extending the stage-2 "delay onset" indication down to age 1, from age 8 and up — a small phase 4 study in under-8s (23 children) supported the expansion.4 Then in June, the FDA granted accelerated approval for children aged 8–17 who have already been diagnosed at stage 3, to slow the decline in their remaining insulin production: per the manufacturer, the first disease-modifying therapy approved for the newly diagnosed. In the PROTECT phase 3 trial (328 participants; 217 on teplizumab, 111 on placebo) the treated group held on to more C-peptide — a marker of the body's own insulin output — by 0.13 pmol/mL on average (95% CI 0.09–0.17; p<0.001).5

    Read that carefully, because the distinctions matter. Accelerated approval is provisional: it rests on a marker (C-peptide) rather than on how people actually feel or fare, and Sanofi must run a confirmatory trial, BETA-PRESERVE, to keep it. Preserving C-peptide did not translate into better day-to-day glucose control in the trial. So the attack can now be bent both before and after diagnosis, across ages 1–17 — which is real, and more than we could say a year ago — but it is still a brake, not a stop.

    The goal worth ranking toward is precision: disarm the specific immune response that targets insulin-producing cells, leave the rest of the immune system intact, and make the effect durable. Antigen-specific and tolerance-restoring approaches that aim at exactly this remain unproven in people. Get there and immunotherapy stops being a way to slow the loss — and becomes the thing that protects every other cure approach.

    References

    1. DiMeglio LA, Evans-Molina C, Oram RA. Type 1 diabetes. Lancet. 2018;391(10138):2449–2462. https://doi.org/10.1016/S0140-6736%2818%2931320-5 ↩

    2. Herold KC, Bundy BN, Long SA, et al. An Anti-CD3 Antibody, Teplizumab, in Relatives at Risk for Type 1 Diabetes. N Engl J Med. 2019;381(7):603–613. https://doi.org/10.1056/NEJMoa1902226 ↩

    3. Sims EK, Bundy BN, Stier K, et al. Teplizumab improves and stabilizes beta cell function in antibody-positive high-risk individuals. Sci Transl Med. 2021;13(583):eabc8980. https://doi.org/10.1126/scitranslmed.abc8980 ↩

    4. Sanofi. Tzield approved in the US to delay the onset of stage 3 type 1 diabetes in children as young as 1 year old. Press release, 22 April 2026. https://www.sanofi.com/en/media-room/press-releases/2026/2026-04-22-05-05-00-3278650 ↩

    5. Sanofi. Tzield approved in the US as the first disease-modifying therapy for patients recently diagnosed with stage 3 type 1 diabetes. Press release, 12 June 2026. https://www.sanofi.com/en/media-room/press-releases/2026/2026-06-12-22-09-58-3311349 ↩

    Our take

    Teplizumab changed the conversation: it proved the timeline is bendable. The prize now is a stop, not a delay — and one precise enough that we're not trading diabetes for a suppressed immune system. The 2026 approvals widen the door; they do not change what is behind it.

    Items working on itAlefacept (CD2 memory T-cell targeting)Baricitinib (JAK1/2 inhibitor)CELZ-201 perinatal tissue-derived cell therapyDimethyl fumarate for beta-cell preservationE-islet 01 allogeneic human regenerative isletsFrexalimab (CD40L antagonist)Golimumab (anti-TNF)Imatinib (tyrosine kinase inhibitor)Low-dose anti-thymocyte globulin (ATG)Minutia (gene-edited hypoimmune islets + graft nanosensors)Mixed haematopoietic chimerism (immune tolerance induction)PIpepTolDC tolerogenic dendritic-cell vaccineRituximab (anti-CD20)SAB-142 (fully human anti-thymocyte globulin)Selective JAK inhibitors (abrocitinib / ritlecitinib)Teplizumab (Tzield)Teplizumab for new-onset T1D (Tzield)Ustekinumab (IL-12/23 p40 blocker)Verapamil (oral)
    Trials advancing itAdaptive platform trial: golimumab in stage 1 (presymptomatic) T1DAllogeneic CD7-targeted CAR-T for T1DAutologous CD6-CAR Tregs for stage-3 T1DCNP-103: tolerogenic nanoparticles in recent-onset T1DDIAGNODE-3: Intralymphatic GAD-alum in HLA DR3-DQ2 recent-onset T1DE-islet 01: allogeneic human regenerative islet therapyENC-201-CED: Encellin encapsulated donor isletsENCRT-103-hPI: Encellin's next-generation encapsulation deviceFABULINUS: Frexalimab CD40L blockade in recent-onset T1DIslet transplantation into the anterior chamber of the eyeIslet transplantation with recipient Tregs or donor bone marrowPrecision ATG with or without verapamil in new-onset T1DPRISE-hATG: SAB-142 in recent-onset and established type 1 diabetesRepeat BCG vaccination in pediatric T1DRESET T1D: rezpegaldesleukin (NKTR-358), a Treg-selective IL-2, in new-onset T1DSAFEGUARD: SAB-142, a fully human anti-thymocyte globulin, in new-onset stage-3 T1DSana SC451: hypoimmune stem-cell-derived islets without immunosuppressionSernova Cell Pouch: implantable islet-transplant scaffoldSingle-center phase 3 islet transplantation in non-uremic T1DTADPOL: DFMO/polyamine pathway in recent-onset T1DTegoprubart: calcineurin-inhibitor-free islet-transplant immunosuppressionVCTX211: CRISPR gene-edited hypoimmune stem-cell isletsWAVE T1D: low-dose ATG followed by adalimumab or verapamil in new-onset T1DAllogeneic regenerative islet transplantation for brittle T1DAllogenic islet cell transplantation at University of ChicagoAutologous Tregs in T1DCARC-101C cell therapy in autoimmune T1DDiamyd GAD-alum in people at risk for T1DDimethyl fumarate for preserving beta-cell function in new-onset T1DGastrin to improve islet transplantation outcomesI-DIT: ixekizumab anti-IL-17 in new-onset T1DIMMUNOSTEM: PD-L1 gene-modified autologous HSPCsIslet transplant with T-cell depletion and gastrinIslet transplantation in brittle T1DIslet transplantation with glucocorticoid-free immunosuppressionMATIN-2: teplizumab, intralymphatic insulin and low-dose IL-2PIpepTolDC tolerogenic dendritic-cell vaccinePOLARIS: GNTI-122 engineered Tregs in recent-onset T1DPROTECT extension: long-term teplizumab safetyRepeat BCG vaccination in established T1DSanofi registry for stage 2 T1D and Tzield treatmentSequential cord-blood stem cells and islets in monogenic immunodeficiency T1DSHIELD-T1D: Shingrix and semaglutide for beta-cell preservationSorafenib in new-onset T1DTeplizumab in Japanese stage-2 T1DTeplizumab in pediatric stage-2 T1DTregs plus anti-CD20 rituximab in pediatric stage 1 T1DTrialNet platform: teplizumab vs low-dose ATG to delay stage-3 T1DAbatacept (CTLA4-Ig) to delay type 1 diabetes in at-risk relativesASK: Autoimmunity Screening for Kids (Colorado)BANDIT: Baricitinib (JAK inhibitor) in recent-onset type 1 diabetesBARICADE-DELAY: Baricitinib to delay stage-3 T1DBARICADE-PRESERVE: Baricitinib in newly diagnosed T1DBETA PRESERVE: confirmatory teplizumab trial in recent-onset stage-3 T1DCREATE-1: CELZ-201 in recent-onset type 1 diabetesDIAGNODE-1: First intralymphatic GAD-alum dosing studyDIAGNODE-2: Intralymphatic GAD-alum (Diamyd) in recent-onset type 1 diabetesDPT-1: Diabetes Prevention Trial-Type 1 (parenteral and oral insulin)ELSA: EarLy Surveillance for Autoimmune diabetes (UK)Fr1da: General-population infant/child islet-autoantibody screening (Bavaria)Imatinib in recent-onset type 1 diabetesJAKPOT T1D: Abrocitinib and ritlecitinib in new-onset T1DLantidra (donislecel): purified allogeneic islet cell therapy (CIT-07)Low-dose anti-thymocyte globulin (ATG) ± GCSF in new-onset T1D (Haller / TrialNet)PROTECT: Teplizumab in children and adolescents with recent-onset type 1 diabetesProtégé: Anti-CD3 (teplizumab) in recent-onset type 1 diabetesRituximab-pvvr followed by abatacept in new-onset T1D (TrialNet T1D RELAY / TN25)T1DAL: Alefacept in new-onset type 1 diabetesT1GER: Golimumab in youth with new-onset type 1 diabetesTN-07: Oral insulin for prevention in autoantibody-positive relativesTN-09: Abatacept (CTLA4-Ig) in recent-onset type 1 diabetesTN-10: Teplizumab to delay clinical type 1 diabetes in at-risk relatives (Stage 2)TN-22: Hydroxychloroquine in stage 1 at-risk individualsTrialNet Pathway to PreventionUST1D2: Ustekinumab phase-2/3 in adults with recent-onset T1DUSTEKID: Ustekinumab in adolescents with recent-onset type 1 diabetesVC-01: ViaCyte first-gen encapsulated stem-cell isletsVCTX210: first CRISPR-edited, device-encapsulated stem-cell islet productVerapamil to preserve beta-cell function in newly diagnosed type 1 diabetes (Ver-A-T1D)VX-264: encapsulated stem-cell islets without immunosuppressionVX-880 / zimislecel: stem-cell-derived islets (with immunosuppression)

  2. A scalable supply of insulin-producing cells

    Replacing what's lost means having insulin-producing cells to transplant. Donor islets are scarce and variable; the breakthrough is growing unlimited, consistent cells from stem cells.

    Editorial estimate of progress55%

    Where we are today

    Stem-cell-derived islet therapy has produced insulin independence in early trials — a genuine milestone. The remaining supply-side problems are manufacturing consistency, scale, and cost, plus making the cells mature and safe (no stray undifferentiated cells). The proof is in the timeline: more than a year after the headline results, the pivotal study is still not complete — its registry primary completion date is mid-2027 — and no regulator has approved the therapy anywhere.

    What would close it

    • Reproducible, GMP-scale differentiation of stem cells into functional islet cells
    • Quality and safety control — ensuring no undifferentiated cells remain
    • Cell sources that sidestep rejection (hypoimmune-engineered or patient-derived lines)
    • Cryopreservation and logistics for an off-the-shelf product

    Open questions

    • Can manufacturing reach the scale and price to treat millions, not dozens?
    • Which cell source wins: universal donor lines, or patient-matched?
    • How mature must lab-grown cells be to regulate glucose like the real thing?
    Read the full picture →

    You can't replace what's been destroyed without a source of replacements. For decades that source was donor pancreases — and conventional islet transplantation is constrained by donor scarcity, variable graft quality, and the need for lifelong immunosuppression.1 As a cure for a disease affecting millions, it was never going to scale.

    Stem cells changed the math. We can now coax stem cells into insulin-producing islet cells in the lab, in principle without limit, and early trials have shown recipients producing their own insulin again — some free of injections entirely. In the zimislecel (VX-880) phase 1–2 trial, all 12 full-dose recipients made glucose-responsive insulin and hit standard glucose targets at one year — HbA1c below 7%, more than 70% time-in-range — and 10 of 12 (83%) no longer needed insulin at all.2 That is one of the most important results in the history of T1D.

    What's left is industrialization: making the cells the same way every time, proving none are left in an immature or risky state, and driving the cost down far enough to matter.3

    The timeline is the evidence for that. More than a year after those headline results, the pivotal study is still not complete — its registry entry lists a primary completion date of June 2027 and no posted results.4 We have seen no announcement of a regulatory filing for zimislecel anywhere, and no regulator has approved it. Vertex's own guidance is for regulatory submissions during 2026 — a plan, not an approval. Nothing about the biology has gone backwards; the slow part is turning a laboratory success into a product you can make, ship and pay for. The supply problem is still closer to solved than any other cure gap — which is exactly why protecting those cells from the immune system is now the rate-limiting step.

    References

    1. Strakosch T, Forbes S. "Navigating the immunological and logistical transformation brought by stem cell-derived islets for the treatment of type 1 diabetes" (UK key-opinion-leader perspective). Diabetic Medicine 2026. Notes that conventional islet transplantation is limited by donor scarcity, variable graft quality, and lifelong immunosuppression, and frames stem-cell-derived islets as a scalable, standardised alternative. https://doi.org/10.1111/dme.70230 ↩

    2. Reichman TW, et al. "Stem Cell–Derived, Fully Differentiated Islets for Type 1 Diabetes" (zimislecel / VX-880 phase 1–2). New England Journal of Medicine 2025;393(9):858–868 (20 June 2025). All 12 full-dose recipients achieved glucose-responsive C-peptide, HbA1c <7% and time-in-range >70% at one year; 10/12 became insulin-independent — all still on immunosuppression. https://doi.org/10.1056/NEJMoa2506549 ↩

    3. Rajaei B, et al. "Clinically compliant enrichment of human pluripotent stem cell-derived islets." Science Translational Medicine 2025;17(792):eadl4390. A scalable, manufacturing-compatible purification step that removes non-target cell types from the final stem-cell-derived islet product. https://doi.org/10.1126/scitranslmed.adl4390 ↩

    4. ClinicalTrials.gov, NCT04786262 — "A Phase 1/2/3 Study to Evaluate the Safety, Tolerability, and Efficacy of VX-880 in Subjects Who Have Type 1 Diabetes Mellitus With Impaired Hypoglycemic Awareness and Severe Hypoglycemia" (sponsor: Vertex Pharmaceuticals). Checked 14 July 2026: enrollment 52, primary completion date 30 June 2027, study completion 2030, no results posted. https://clinicaltrials.gov/study/NCT04786262 ↩

    Our take

    This is the cure gap with the most visible momentum. Insulin independence from lab-grown cells has happened in humans. The fight has moved from "can we make the cells" to "can we make them by the million, safely, and protect them" — see encapsulation and the immune attack.

    Items working on itAspect Biosystems bioprinted islet tissue (ex-Novo Nordisk platform)Beta-cell regeneration / regrowth agentsCentury Therapeutics CNTY-813 (Allo-Evasion 5.0 iPSC islets)CiPSC-derived autologous islets (RGB-5088)E-islet 01 allogeneic human regenerative isletsIcovamenib (BMF-219) — oral menin inhibitorOZTx-410 allogeneic iPSC islet cell sheet (Orizuru)SIG-002 (Lilly/Sigilon Afibromer-encapsulated islets)
    Trials advancing itCOVALENT-112: icovamenib (oral menin inhibitor) in type 1 diabetesE-islet 01: allogeneic human regenerative islet therapyiPSC-derived islet cells for diabetes (Peking University First Hospital)OPF-310 encapsulated porcine islets for unstable T1DRGB-5088 autologous CiPSC-derived islet injection in T1DSana SC451: hypoimmune stem-cell-derived islets without immunosuppressionSernova Cell Pouch: implantable islet-transplant scaffoldVCTX211: CRISPR gene-edited hypoimmune stem-cell isletsVX-880 / zimislecel: phase 3 in T1D with a kidney transplantAllogeneic regenerative islet transplantation for brittle T1DAllogenic islet cell transplantation at University of ChicagoAutologous insulin-producing mesenchymal stem cells in youthCelregen CRG-002 allogeneic iPSC-derived isletsIslet transplantation in brittle T1DSequential cord-blood stem cells and islets in monogenic immunodeficiency T1DSeraxis SR-02 pancreatic endocrine cells in adult T1DLantidra (donislecel): purified allogeneic islet cell therapy (CIT-07)VC-01: ViaCyte first-gen encapsulated stem-cell isletsVCTX210: first CRISPR-edited, device-encapsulated stem-cell islet productVX-264: encapsulated stem-cell islets without immunosuppressionVX-880 / zimislecel: stem-cell-derived islets (with immunosuppression)

  3. Protecting cells without lifelong immunosuppression

    Transplanted cells face two enemies: the original autoimmune attack and ordinary transplant rejection. Today the defense is immunosuppressant drugs for life — which is why cell therapy is reserved for the most severe cases. Remove that requirement and a cure opens to everyone.

    Editorial estimate of progress30%

    Where we are today

    Set the bar honestly and the field gets very small. "Immunosuppression-free" means no chronic systemic anti-rejection drugs at all — not a gentler regimen, not a calcineurin-free one. By that bar, as of July 2026 exactly one person on earth is living with transplanted insulin-producing cells and zero immunosuppression: the single participant in Sana's UP421 study, whose gene-edited donor islets were still making C-peptide at 14 months (NEJM, July 2026). He received a deliberately sub-therapeutic dose and is still on insulin. That is the entire human evidence base. Everything else that claims to be drug-free is preclinical — and the past year went badly. Vertex discontinued VX-264, the best-funded encapsulation device (the cells were safe but never produced enough C-peptide to help, consistent with hypoxia and fibrosis inside the capsule), and the CRISPR/ViaCyte hypoimmune Phase 1, VCTX211, was terminated after five participants; CRISPR has fallen back to a preclinical candidate, CTX213. In January 2026 Novo Nordisk exited in-house cell therapy altogether, handing its stem-cell-islet and hypoimmune platforms to Aspect Biosystems. The next genuine clinical shot is Century's CNTY-813, with an IND targeted for Q4 2026 and first data guided to 2H 2027.

    What would close it

    • Encapsulation materials that solve the two failures that killed the devices — oxygen supply to the cell core, and foreign-body fibrosis walling the capsule off
    • Hypoimmune cell engineering that survives rejection AND recurrent autoimmunity without drugs — the second half is the part that is still unproven
    • Engineering around the NK-cell problem — a cell hidden from T cells by deleting HLA becomes a target for natural killer cells, which hunt exactly that
    • Built-in safety switches (e.g. inducible kill genes) for cells deliberately made invisible to immune surveillance
    • Local immune modulation at the implant site instead of body-wide drugs
    • Less-toxic immunosuppression as a bridge — real progress, but it does not clear this bar and we do not score it as if it did

    Open questions

    • Can a capsule keep cells oxygenated and un-fibrosed for years? Both best-funded attempts failed on exactly this, and no one has shown otherwise in a human.
    • Does immune cloaking hold against recurrent autoimmunity — the memory T cells that destroyed the person's own beta cells — and not just against generic rejection? Autologous grafts are perfectly matched and autoimmunity attacks them anyway. This is the problem everyone forgets.
    • If you hide a cell from T cells, what stops NK cells from killing it instead?
    • A cell invisible to immune surveillance is also invisible to cancer surveillance. What is the plan when an engineered graft goes wrong?
    • Does the one 14-month result hold at a therapeutic dose, in more than one person? Survival at a sub-therapeutic dose is not the same claim as function at a curative one.
    • If protection fails silently, how does the person know before the graft is lost?
    Read the full picture →

    Here is the cruel catch in cell-replacement therapy: the cells work, but keeping them alive means suppressing the immune system for life. The drugs carry real risks — infection, cancer, organ strain — heavy enough that the therapy is reserved for people with the most dangerous, uncontrollable T1D. The cure exists; it's just locked behind a trade most people shouldn't make.

    First, the bar

    This page is strict about one phrase, because the field is not. "Immunosuppression-free" means no chronic systemic anti-rejection drugs. Full stop. Three things that are routinely sold as clearing that bar do not:

    • A gentler regimen is not no regimen. Dropping calcineurin inhibitors is a real gain in safety, but a drug like anti-CD40L (tegoprubart) is still chronic systemic immunosuppression. This is the single most common overclaim in beta-cell replacement.
    • Using the patient's own cells is not drug-free. Autologous cells solve rejection. They do nothing about the autoimmunity that caused T1D in the first place — a perfectly matched graft still gets attacked by the memory T cells that destroyed the original beta cells. Both celebrated Chinese "cured with their own cells" cases were in people already on chronic systemic immunosuppression for a previous solid-organ transplant: the CiPSC-islet patient in Tianjin had had a liver transplant, and the team said plainly that this let them "leverage existing immunosuppressive therapy";12 the E-islet patient in Shanghai had had a kidney transplant — and had type 2 diabetes, not type 1.3 Nobody has yet shown a graft of a person's own reprogrammed islets surviving in an untreated T1D immune system.
    • Transplanting nothing is not solving protection. A therapy that needs no anti-rejection drugs because it implants no cells has dodged the question, not answered it.

    And a mouse result is not a human result. A goal is not an achievement. We do not score intentions.

    Where that leaves us: n=1

    Apply the bar and the human evidence base for drug-free cell replacement is one person. In Sana's UP421 study, gene-edited (hypoimmune) donor islets were transplanted into a man with T1D who took no immunosuppression at all. At 14 months they were still producing C-peptide — fasting and meal-stimulated levels comparable to the first six months and higher than at months 9 and 12, from an undetectable baseline — and a 52-week PET-MRI still showed the graft alive at the forearm implant site, with no safety problems reported.4

    That is a genuinely important result and it is worth being precise about what it is. One participant. A deliberately sub-therapeutic dose of cells. A study never designed to lower his insulin or improve his glucose control — and it didn't; he is still on insulin. What it tested is narrower and, for this gap, exactly the right question: can immune-cloaked cells from a stranger survive in an unprotected immune system for more than a year? So far, in this one man, yes. That is proof of survival, not proof of cure, and the distance between those two words is the whole remaining problem.5

    Everything else that claims to be drug-free is preclinical. Hypoimmune islets did reach insulin independence with no immunosuppression in a fully immunocompetent monkey6 — encouraging, and still not a person.

    The year the leading programmes died

    A roadmap that only records good news is useless. Between them, the two best-funded attempts at drug-free protection both failed, and a major pharma walked out.

    Encapsulation lost its lead candidate. Vertex's VX-264 put islet cells inside an immunoprotective device meant to need no immunosuppression. The cells were safe; they simply never produced enough C-peptide to help anyone, and the programme was discontinued in March 2025.7 The likely reasons are the two failure modes that have dogged this route for decades: cells at the core of a capsule suffocate for want of oxygen, and the body walls the capsule off in fibrous scar tissue, cutting off the nutrient exchange the design depends on. There is now no credible late-stage clinical programme for the physical-barrier route.

    The hypoimmune-in-a-device trial was terminated. CRISPR Therapeutics' VCTX211, gene-edited immune-evasive cells in a retrievable device, is listed on the registry as TERMINATED after five participants, with no results posted.8 CRISPR has retreated to a preclinical, deviceless successor, CTX213.9

    Novo Nordisk left. In January 2026 Novo handed its stem-cell-derived islet and hypoimmune platforms to Aspect Biosystems, following its decision to discontinue in-house cell therapy R&D.10 Partnerships get spun as progress; a company of Novo's size exiting a field is a retreat, and we will call it one.

    The next real shot on goal is Century Therapeutics' CNTY-813, an allogeneic iPSC-derived islet therapy engineered for engraftment without chronic systemic immunosuppression. It is preclinical today, with an IND targeted for Q4 2026 and first clinical data guided to 2H 2027.11

    What still has to be solved

    The failure modes are, at least, now well characterised — which is its own kind of progress:

    • Hypoxia and fibrosis kill encapsulated cells. Nobody has beaten both in a human.
    • Hide from T cells and you meet the NK cells. Deleting HLA to escape T-cell recognition is exactly the "missing self" signal natural killer cells are built to hunt. The cloak creates its own predator.
    • A cell invisible to immune surveillance is invisible to cancer surveillance too. Engineering a graft the body cannot see is engineering a graft the body cannot police.
    • Recurrent autoimmunity attacks even a perfectly matched autologous graft. This is the one the field keeps forgetting, and it is the reason "your own cells" is not an answer here.

    A third route, honestly labelled: gentler drugs, not no drugs

    Alongside the drug-free ambition, a more modest strategy is making real clinical progress: keep immunosuppression, but strip out its most damaging parts. At ADA 2026, an islet-transplant trial using an investigational immunotherapy from Eledon reported that all 12 participants were able to stop using insulin, with no severe safety concerns.12 Those people are still on immunosuppressive drugs. This is not a drug-free cure and we will not file it as one — but if the regimen is meaningfully safer than today's, it widens the door in the meantime while cloaking and encapsulation mature.13

    Whoever solves protection — fully, durably, drug-free, at a dose that actually cures — turns a niche procedure into a cure the whole T1D population can have. Nobody has done it yet.

    References

    1. Wang S, Du Y, Zhang B, et al. "Transplantation of chemically induced pluripotent stem-cell-derived islets under abdominal anterior rectus sheath in a type 1 diabetes patient." Cell 187(22):6152-6164 (2024). One patient, autologous CiPSC islets, insulin-independent from day 75 and still off insulin at one year — an important result, in a woman who had already received a liver transplant and was on chronic systemic immunosuppression for it. https://doi.org/10.1016/j.cell.2024.09.004 ↩

    2. Lou Y. "Illuminating the future of diabetes treatment: Autologous CiPSC-derived islets take center stage." Cell Transplantation (2025): "The first human trial involved a patient with a history of liver transplantation, allowing the team to leverage existing immunosuppressive therapy." https://doi.org/10.1177/09636897251366828 ↩

    3. Wu J, Li T, Guo M, et al. "Treating a type 2 diabetic patient with impaired pancreatic islet function by personalized endoderm stem cell-derived islet tissue." Cell Discovery (2024): "The patient was a 59-year-old man with a 25-year history of T2D who developed end-stage diabetic nephropathy and underwent kidney transplantation in June of 2017." Already immunosuppressed, and not type 1 diabetes. https://doi.org/10.1038/s41421-024-00662-3 ↩

    4. Follow-on peer-reviewed Letter to the Editor in the New England Journal of Medicine, announced 13 July 2026: in the UP421 study, hypoimmune (HIP) gene-edited allogeneic islets transplanted without any immunosuppression were still secreting C-peptide at 14 months — fasting and meal-stimulated levels comparable to the first six months and exceeding months 9 and 12, from an undetectable baseline — with a 52-week PET-MRI confirming surviving islet cells at the forearm site and no safety issues. A single participant, given a deliberately low cell dose, in a study explicitly not designed to improve glucose control or reduce insulin use. Sana Biotechnology press release (13 July 2026). https://www.globenewswire.com/news-release/2026/07/13/3326134/0/en/Sana-Biotechnology-Announces-Follow-On-Publication-in-The-New-England-Journal-of-Medicine-NEJM-Highlighting-Groundbreaking-Long-Term-Data-and-Durability-of-Hypoimmune-Modified-Isle.html ↩

    5. First-in-human case report: hypoimmune (HIP) gene-edited allogeneic islet cells survived and secreted insulin (C-peptide), responding to a meal, in a person with type 1 diabetes without any immunosuppression. "Survival of Transplanted Allogeneic Beta Cells with No Immunosuppression," New England Journal of Medicine (2025). https://doi.org/10.1056/NEJMoa2503822 ↩

    6. In a fully immunocompetent, diabetic non-human primate, allogeneic hypoimmune (B2M and CIITA knockout, CD47 overexpression) islets engrafted and provided stable insulin independence with no detectable immune response and no immunosuppression — preclinical proof of the "cloak" approach. Hu X, et al., "Hypoimmune islets achieve insulin independence after allogeneic transplantation in a fully immunocompetent non-human primate," Cell Stem Cell (2024). https://doi.org/10.1016/j.stem.2024.02.001 ↩

    7. Vertex's lead encapsulation candidate VX-264 — islet cells inside an immunoprotective device requiring no immunosuppression — was safe, but C-peptide did not rise to levels that would deliver clinical benefit, and the programme was discontinued in March 2025. Vertex Pharmaceuticals, "Vertex Announces Program Updates for its Type 1 Diabetes Portfolio" (2025). https://investors.vrtx.com/news-releases/news-release-details/vertex-announces-program-updates-type-1-diabetes-portfolio ↩

    8. VCTX211 (NCT05565248), a CRISPR Therapeutics / ViaCyte Phase 1 first-in-human study of CRISPR/Cas9-edited, immune-evasive pancreatic endoderm cells in a durable retrievable device, is listed on ClinicalTrials.gov with status TERMINATED — enrolment 5, completion 8 August 2025, no results posted. https://clinicaltrials.gov/study/NCT05565248 ↩

    9. CRISPR Therapeutics describes CTX213 — a deviceless beta-cell replacement candidate using edited iPSC-derived islet cells — as showing preclinical efficacy and "progressing toward the clinic," i.e. it is not yet in human testing. CRISPR Therapeutics, Q1 2026 business update (4 May 2026). https://www.globenewswire.com/news-release/2026/05/04/3287176/0/en/crispr-therapeutics-provides-business-update-and-reports-first-quarter-2026-financial-results.html ↩

    10. On 20 January 2026 Aspect Biosystems announced it had acquired Novo Nordisk's stem-cell-derived islet and hypoimmune cell-engineering technologies, following Novo's decision to discontinue in-house cell therapy research and development. Novo retains investment, research funding, and future commercialisation/royalty options. https://www.aspectbiosystems.com/news-resources/aspect-biosystems-novo-nordisk-enter-new-phase-of-partnership-to-develop-curative-medicines-for-diabetes ↩

    11. CNTY-813 is an allogeneic iPSC-derived islet replacement therapy engineered with Century's Allo-Evasion 5.0, "designed to enable durable engraftment without chronic systemic immunosuppression." It is preclinical: Century is targeting an IND submission in Q4 2026, with initial clinical data expected in 2H 2027. Century Therapeutics (9 July 2026). https://www.globenewswire.com/news-release/2026/07/09/3324741/0/en/Century-Therapeutics-Selected-for-Oral-Presentations-of-CNTY-813-Preclinical-Data-at-EASD-2026-and-Breakthrough-T1D-Clinical-Research-Congress-2026.html ↩

    12. Reported at the ADA 2026 Scientific Sessions: all 12 participants who received islet transplants under an investigational immunotherapy regimen from Eledon Pharmaceuticals were able to stop using insulin, with no severe safety concerns. These recipients remain on chronic systemic immunosuppression — the aim is a less toxic regimen, not the elimination of immunosuppression, and it does not clear the bar this page sets. Breakthrough T1D, "Highlights from ADA 2026 Scientific Sessions" (2026). https://breakthrought1d.ca/highlights-from-ada-2026-scientific-sessions/ ↩

    13. A 2025 review of the field describes encapsulation and gene editing to create hypoimmune cells as the strategies that "could reduce the need for immunosuppression that has hampered β-cell replacement." Ziegler AG, Cengiz E, Kay TWH, "The future of type 1 diabetes therapy," Lancet (2025). https://doi.org/10.1016/S0140-6736%2825%2901438-2 ↩

    Our take

    We are lowering this from 35 to 30, and we want to be explicit about why, because a number that only ever goes up is a marketing device, not an estimate. The science did learn something real this year: the Sana participant is the first human ever to keep transplanted insulin-producing cells alive with no immunosuppression at all, and 14 months is genuine durability. But 35 implicitly priced in two live clinical routes racing each other. Now there is one. Encapsulation has no credible clinical programme left after VX-264; CRISPR's hypoimmune device trial was terminated and the programme is back in preclinical; Novo Nordisk left the field. What remains, in humans, is n=1 at a dose chosen not to cure anyone. The gap is no closer to being *closed* than it was a year ago, and the route to a patient got longer. That is a decrease. This remains the true gate on a universal cure: we have cells that work and a growing supply of them, and still no way to protect them that is good enough to skip the drugs. Watch CNTY-813's IND and a therapeutic-dose hypoimmune study — those, not press releases, are what would move this number back up.

    Items working on itAspect Biosystems bioprinted islet tissue (ex-Novo Nordisk platform)Century Therapeutics CNTY-813 (Allo-Evasion 5.0 iPSC islets)iTolerance iTOL-102 (SA-FasL microgel + islets)Minutia (gene-edited hypoimmune islets + graft nanosensors)MIT oxygen-generating encapsulation device (self-oxygenating islet implant)Mixed haematopoietic chimerism (immune tolerance induction)SIG-002 (Lilly/Sigilon Afibromer-encapsulated islets)ViCapsys / MGH CXCL12-alginate islet encapsulation (VICAPSYN)
    Trials advancing itENC-201-CED: Encellin encapsulated donor isletsENCRT-103-hPI: Encellin's next-generation encapsulation deviceOPF-310 encapsulated porcine islets for unstable T1DSana SC451: hypoimmune stem-cell-derived islets without immunosuppressionVCTX211: CRISPR gene-edited hypoimmune stem-cell isletsVX-880 / zimislecel: phase 3 in T1D with a kidney transplantSeraxis SR-02 pancreatic endocrine cells in adult T1DAbatacept (CTLA4-Ig) to delay type 1 diabetes in at-risk relativesDIAGNODE-1: First intralymphatic GAD-alum dosing studyDIAGNODE-2: Intralymphatic GAD-alum (Diamyd) in recent-onset type 1 diabetesDPT-1: Diabetes Prevention Trial-Type 1 (parenteral and oral insulin)Lantidra (donislecel): purified allogeneic islet cell therapy (CIT-07)Low-dose anti-thymocyte globulin (ATG) ± GCSF in new-onset T1D (Haller / TrialNet)PROTECT: Teplizumab in children and adolescents with recent-onset type 1 diabetesProtégé: Anti-CD3 (teplizumab) in recent-onset type 1 diabetesRituximab-pvvr followed by abatacept in new-onset T1D (TrialNet T1D RELAY / TN25)TN-07: Oral insulin for prevention in autoantibody-positive relativesTN-09: Abatacept (CTLA4-Ig) in recent-onset type 1 diabetesTN-10: Teplizumab to delay clinical type 1 diabetes in at-risk relatives (Stage 2)TN-22: Hydroxychloroquine in stage 1 at-risk individualsVC-01: ViaCyte first-gen encapsulated stem-cell isletsVCTX210: first CRISPR-edited, device-encapsulated stem-cell islet productVerapamil to preserve beta-cell function in newly diagnosed type 1 diabetes (Ver-A-T1D)VX-264: encapsulated stem-cell islets without immunosuppressionVX-880 / zimislecel: stem-cell-derived islets (with immunosuppression)

  4. Finding it early enough to act

    The interventions that preserve the body's own insulin production work best before most cells are gone — but most people are diagnosed only at crisis, in the ER, with little left to save. You can't protect what's already destroyed.

    Editorial estimate of progress45%

    Where we are today

    A simple autoantibody test can identify T1D years before symptoms and stage how far it's progressed. General-population screening programs are expanding — the UK's ELSA study has now reported that screening children in the general population is feasible — and early detection already slashes dangerous DKA-at-diagnosis. What a positive result leads to has grown too: in 2026 US regulators approved teplizumab (Tzield) from age 1 at stage 2, and then for children recently diagnosed at stage 3. But screening is still far from universal, so the therapeutic window is usually missed.

    What would close it

    • Low-cost, scalable screening (home and capillary tests) for the general population, not just relatives
    • Integrating screening into routine pediatric and primary care
    • Better staging and progression prediction to time interventions
    • Linking a positive screen directly to monitoring and trial access

    Open questions

    • How do you screen a whole population affordably and equitably?
    • How often must someone at risk be re-tested as the disease evolves?
    • Can we predict not just *if* but *when* clinical onset will hit?
    Read the full picture →

    There's a window in T1D when intervention pays off most: while the body still has a meaningful share of its insulin-producing cells. Protect them then and a person may keep partial insulin production for years — easier control, fewer complications, more time for better cures to arrive. Miss it and you're rebuilding from zero.

    The tragedy is that most people are found at the very end of that window — diagnosed in the emergency room, often in diabetic ketoacidosis, with little left to save. Yet a simple test for autoantibodies can flag the disease years earlier and even stage how far along it is.

    The gap is reach. Screening has mostly been offered to relatives of people with T1D — but roughly 90% of new cases have no family history, so that misses the majority.1 Universal, low-cost screening built into routine care would change who gets found, and when: in the Bavarian Fr1da program, children identified pre-symptomatically had DKA at clinical onset in only ~2.5% of cases — far below the roughly 20–48% range reported at unscreened clinical onset.2 It's the cheapest intervention on this page, and it's the one that makes every other cure-strand advance actually reachable for real people.

    The reach problem is being chipped at. The UK's ELSA study has now reported, in a research letter, that offering autoantibody screening to children in the general population — not just relatives — is feasible.3 That is a feasibility finding, not proof that a national program works or pays for itself; those questions are still open. But it moves the argument from "could this ever be done outside a research setting?" to "how do we do it at scale?"

    What has changed most in 2026 is the payoff for finding someone. Until recently, a positive screen in a young child mostly bought you monitoring and a heads-up. Now, in the US, teplizumab (Tzield) is approved from age 1 for stage 2 — the presymptomatic stage a screen actually catches4 — and, since June 2026, for children aged 8–17 who have just been diagnosed at stage 3.5 Both of those are US decisions, and the stage-3 one is an accelerated approval, so confirmatory evidence is still owed. Still, the practical picture has shifted: a positive result now leads somewhere at almost any age, and being found at stage 3 is no longer a dead end for preserving what's left.

    None of that fixes the gap itself. Screening reach has not meaningfully moved — the therapeutic window is still missed for most people, which is why this gap's progress score hasn't budged. It just means the cost of missing it is higher than it used to be.

    References

    1. Approximately 90% of people who develop T1D have no first-degree relative with the disease, so screening only relatives misses most future cases — a key rationale for general-population screening. Sims EK, et al. "Screening for Type 1 Diabetes in the General Population: A Status Report and Perspective." Diabetes 71(4):610–623 (2022). https://doi.org/10.2337/dbi20-0054 ↩

    2. The Fr1da study screened 90,632 Bavarian children for islet autoantibodies in routine primary care, detecting presymptomatic T1D at 0.31% prevalence with only 2 cases of DKA among those identified. Ziegler A-G, et al. "Yield of a Public Health Screening of Children for Islet Autoantibodies in Bavaria, Germany." JAMA 323(4):339–351 (2020). https://doi.org/10.1001/jama.2019.21565. Children diagnosed pre-symptomatically then went on to milder clinical onset, with DKA in only 2.5% versus the ~20–48% generally reported at unscreened clinical onset. Hummel S, et al. "Children diagnosed with presymptomatic type 1 diabetes through public health screening have milder diabetes at clinical manifestation." Diabetologia 66(9):1633–1642 (2023). https://doi.org/10.1007/s00125-023-05953-0 ↩

    3. A research letter — a short report, not a full trial — describing the UK ELSA study's experience offering general-population childhood autoantibody screening, and concluding it is feasible. Quinn LM, Narendran P, et al. "Feasibility of general population screening for type 1 diabetes in the UK: the ELSA study." Lancet Diabetes & Endocrinology 14(3):197–199 (2026). https://doi.org/10.1016/S2213-8587(25)00363-8 ↩

    4. In April 2026 Sanofi announced that the US label for Tzield (teplizumab) was expanded to include children from age 1 with stage 2 T1D, lowering the age floor for acting on a positive presymptomatic screen. Manufacturer press release, 22 April 2026. https://www.sanofi.com/en/media-room/press-releases/2026/2026-04-22-05-05-00-3278650 ↩

    5. In June 2026 Sanofi announced a US accelerated approval of Tzield for children aged 8–17 recently diagnosed with stage 3 T1D — the first disease-modifying therapy for people already at clinical onset. Accelerated approval means confirmatory evidence is still required; this is a manufacturer announcement, not a published trial report. Manufacturer press release, 12 June 2026. https://www.sanofi.com/en/media-room/press-releases/2026/2026-06-12-22-09-58-3311349 ↩

    Our take

    The most underrated lever on the whole cure roadmap, because it multiplies everything else: every prevention therapy, every cell-preserving immunotherapy, is only as useful as our ability to find people while they still have something to preserve. Screening is cheap. Missing the window is not. And in 2026 the payoff for finding someone got bigger: in the US there is now an approved therapy from age 1, so a positive screen leads somewhere at almost any age.

    Items working on itASK (Autoimmunity Screening for Kids)Australian T1D National Screening PilotD1Ce Screen / Italy national screening (Law 130/2023)EDENT1FI (European early-detection consortium)Golimumab (anti-TNF)Low-dose anti-thymocyte globulin (ATG)Oral glucose tolerance test (OGTT) for T1D stagingRituximab (anti-CD20)T1DRA (Type 1 Diabetes Risk in Adults)Teplizumab (Tzield)
    Trials advancing itAdaptive platform trial: golimumab in stage 1 (presymptomatic) T1DDiamyd GAD-alum in people at risk for T1DGLP-1 receptor agonist for stage-1 T1DGLP-1RA added around teplizumab in stage-2 T1DGTT@Home: home oral glucose tolerance testing for T1D screeningQuebec screening program for relatives of people with T1DSanofi registry for stage 2 T1D and Tzield treatmentTeplizumab in Japanese stage-2 T1DTeplizumab in pediatric stage-2 T1DTregs plus anti-CD20 rituximab in pediatric stage 1 T1DTrialNet platform: teplizumab vs low-dose ATG to delay stage-3 T1DType 1 diabetes screening in pediatric primary careAbatacept (CTLA4-Ig) to delay type 1 diabetes in at-risk relativesASK: Autoimmunity Screening for Kids (Colorado)BARICADE-DELAY: Baricitinib to delay stage-3 T1DDPT-1: Diabetes Prevention Trial-Type 1 (parenteral and oral insulin)ELSA: EarLy Surveillance for Autoimmune diabetes (UK)Fr1da: General-population infant/child islet-autoantibody screening (Bavaria)Protégé: Anti-CD3 (teplizumab) in recent-onset type 1 diabetesTN-07: Oral insulin for prevention in autoantibody-positive relativesTN-10: Teplizumab to delay clinical type 1 diabetes in at-risk relatives (Stage 2)TN-22: Hydroxychloroquine in stage 1 at-risk individualsTrialNet Pathway to Prevention

  5. Making a cure last a lifetime

    A cure that fades in a few years is a reprieve, not a cure. Restored insulin production has to survive the ongoing autoimmunity, the wear on the cells, and the years — ideally for decades, ideally once.

    Editorial estimate of progress20%

    Where we are today

    Early islet and stem-cell results show function can be restored; how long it lasts at scale, and whether it holds without continuous drugs, is still being learned. The longest peer-reviewed follow-up for the leading stem-cell therapy remains about one year. The longest drug-free follow-up is 14 months — in a single person, at a low dose, in a study never designed to reduce insulin use. Regeneration and gene approaches that could refresh or renew cells in place are earlier still.

    What would close it

    • Long-term follow-up on graft survival and insulin independence
    • Regeneration — coaxing the body to regrow its own insulin-producing cells
    • Strategies to refresh or top up grafts non-invasively over time
    • Protecting restored cells from the same autoimmunity that caused T1D

    Open questions

    • How many years can a single cell-replacement procedure last?
    • Can the body be made to regenerate insulin-producing cells durably on its own?
    • Is "functional cure" (stable, drug-light control) the realistic near-term goal, with one-and-done further out?
    Read the full picture →

    The word "cure" carries a promise: not just that something works, but that it lasts. For T1D that bar is steep. Whatever restores insulin production has to withstand the autoimmunity that caused the disease in the first place, the ordinary aging and exhaustion of working cells, and simply the passage of decades. A therapy that delivers two good years is a meaningful treatment — but calling it a cure would be the kind of overstatement this site exists to avoid. The most advanced cell therapy so far, zimislecel, has reported glucose-responsive insulin production durable only through about one year of follow-up — promising, but nowhere near the decades a true cure implies.1

    A second clock is running alongside that one: how long restored cells last without immunosuppressive drugs. In July 2026 Sana reported that its hypoimmune-modified islet cells were still producing meal-responsive C-peptide 14 months after transplant, with no immunosuppression at any point, and imaging at 52 weeks confirming the graft was still there. That is the longest drug-free follow-up anyone has reported — and it is one person, at a deliberately low dose, in a study that was never designed to reduce anyone's insulin use.2 It is a genuinely encouraging signal about whether hidden cells can survive the immune system over time. It is not evidence that a cure lasts, and we are not treating it as one.

    There's a useful distinction here. A functional cure means stable, near-normal glucose with little or no day-to-day burden — even if it leans on a long-lived implant or occasional drugs. A complete cure means the body simply regulates glucose on its own again, indefinitely, ideally from a single intervention. The first is within sight; the second is the longer horizon, where regeneration and gene approaches live — and where the recurring obstacles are durable graft survival and the immune system, both the original autoimmunity and the response to the transplant itself.3

    Durability is also where intellectual honesty matters most. Early results deserve excitement, not coronation. Our job is to show how long each approach has actually been shown to last — and to rank a lasting answer above a temporary one, every time.

    References

    1. In the zimislecel (VX-880) phase 1–2 trial, all 14 participants engrafted and produced C-peptide, and 10 of 12 who received the full dose were insulin-independent at day 365; the authors describe this as a "small, short-term study," with islet function followed through about one year — the longest reported data for a stem-cell islet therapy and a reminder that long-term durability is still unproven. Reichman TW, et al. New England Journal of Medicine (2025). https://doi.org/10.1056/NEJMoa2506549 ↩

    2. Reported by Sana Biotechnology (2026-07-13) as a follow-on peer-reviewed Letter to the Editor in the New England Journal of Medicine — a short correspondence update, not a full trial paper. C-peptide at month 14 was comparable to months 1–6 and higher than at months 9 and 12, and 52-week PET-MRI confirmed the graft at the forearm site. Important limits: a single participant, a low cell dose, and a study not powered or designed to reduce exogenous insulin. https://www.globenewswire.com/news-release/2026/07/13/3326134/0/en/Sana-Biotechnology-Announces-Follow-On-Publication-in-The-New-England-Journal-of-Medicine-NEJM-Highlighting-Groundbreaking-Long-Term-Data-and-Durability-of-Hypoimmune-Modified-Isle.html ↩

    3. Reviews of the field place sustained, long-term graft function and freedom from chronic immunosuppression as the "next frontier," with strategies such as immune-isolation, immune-privileged sites, immune-evasive gene editing, and tolerance induction all still under investigation. Hering BJ, Rickels MR, et al., "Advances in Cell Replacement Therapies for Diabetes," Diabetes (2025). https://doi.org/10.2337/db25-0037 — and across recent trials, durable insulin independence and immune rejection remain the key unsolved challenges: Lin TM, et al., Diabetes & Metabolism (2026). https://doi.org/10.1016/j.diabet.2026.101738 ↩

    Our take

    The honesty gap. It's tempting to call the first insulin-independence results a cure — but durability is unproven, and saying so plainly is the whole point of this site. We rank a five-year fix below a lifetime one, and we say which is which.

    Items working on itAlefacept (CD2 memory T-cell targeting)Aspect Biosystems bioprinted islet tissue (ex-Novo Nordisk platform)Beta-cell regeneration / regrowth agentsCELZ-201 perinatal tissue-derived cell therapyCentury Therapeutics CNTY-813 (Allo-Evasion 5.0 iPSC islets)CiPSC-derived autologous islets (RGB-5088)Denosumab beta-cell preservationDimethyl fumarate for beta-cell preservationE-islet 01 allogeneic human regenerative isletsFrexalimab (CD40L antagonist)GLP-1 drugs to rescue beta cells at diagnosisGolimumab (anti-TNF)Icovamenib (BMF-219) — oral menin inhibitorImatinib (tyrosine kinase inhibitor)iTolerance iTOL-102 (SA-FasL microgel + islets)Minutia (gene-edited hypoimmune islets + graft nanosensors)MIT oxygen-generating encapsulation device (self-oxygenating islet implant)Mixed haematopoietic chimerism (immune tolerance induction)OZTx-410 allogeneic iPSC islet cell sheet (Orizuru)SAB-142 (fully human anti-thymocyte globulin)Selective JAK inhibitors (abrocitinib / ritlecitinib)Sernova Cell Pouch Bio-hybrid OrganSIG-002 (Lilly/Sigilon Afibromer-encapsulated islets)Teplizumab for new-onset T1D (Tzield)Ustekinumab (IL-12/23 p40 blocker)Verapamil (oral)ViCapsys / MGH CXCL12-alginate islet encapsulation (VICAPSYN)
    Trials advancing itCNP-103: tolerogenic nanoparticles in recent-onset T1DCOVALENT-112: icovamenib (oral menin inhibitor) in type 1 diabetesDIAGNODE-3: Intralymphatic GAD-alum in HLA DR3-DQ2 recent-onset T1DE-islet 01: allogeneic human regenerative islet therapyENC-201-CED: Encellin encapsulated donor isletsENCRT-103-hPI: Encellin's next-generation encapsulation deviceFABULINUS: Frexalimab CD40L blockade in recent-onset T1DiPSC-derived islet cells for diabetes (Peking University First Hospital)Islet transplantation into the anterior chamber of the eyeIslet transplantation with recipient Tregs or donor bone marrowOPF-310 encapsulated porcine islets for unstable T1DPrecision ATG with or without verapamil in new-onset T1DPRISE-hATG: SAB-142 in recent-onset and established type 1 diabetesRepeat BCG vaccination in pediatric T1DRESET T1D: rezpegaldesleukin (NKTR-358), a Treg-selective IL-2, in new-onset T1DRGB-5088 autologous CiPSC-derived islet injection in T1DSAFEGUARD: SAB-142, a fully human anti-thymocyte globulin, in new-onset stage-3 T1DSana SC451: hypoimmune stem-cell-derived islets without immunosuppressionSernova Cell Pouch: implantable islet-transplant scaffoldSingle-center phase 3 islet transplantation in non-uremic T1DTADPOL: DFMO/polyamine pathway in recent-onset T1DTegoprubart: calcineurin-inhibitor-free islet-transplant immunosuppressionVCTX211: CRISPR gene-edited hypoimmune stem-cell isletsVX-880 / zimislecel: phase 3 in T1D with a kidney transplantWAVE T1D: low-dose ATG followed by adalimumab or verapamil in new-onset T1DAllogeneic regenerative islet transplantation for brittle T1DAllogenic islet cell transplantation at University of ChicagoAutologous insulin-producing mesenchymal stem cells in youthCARC-101C cell therapy in autoimmune T1DCelregen CRG-002 allogeneic iPSC-derived isletsDenosumab for beta-cell function in T1DDimethyl fumarate for preserving beta-cell function in new-onset T1DGastrin to improve islet transplantation outcomesGLP-1 receptor agonist for stage-1 T1DGLP-1RA added around teplizumab in stage-2 T1DI-DIT: ixekizumab anti-IL-17 in new-onset T1DIMMUNOSTEM: PD-L1 gene-modified autologous HSPCsIslet transplant with T-cell depletion and gastrinIslet transplantation in brittle T1DIslet transplantation with glucocorticoid-free immunosuppressionMATIN-2: teplizumab, intralymphatic insulin and low-dose IL-2MTX228 adaptive phase 2 study in T1DPOLARIS: GNTI-122 engineered Tregs in recent-onset T1DPROTECT extension: long-term teplizumab safetyRepeat BCG vaccination in established T1DSanofi registry for stage 2 T1D and Tzield treatmentSequential cord-blood stem cells and islets in monogenic immunodeficiency T1DSeraxis SR-02 pancreatic endocrine cells in adult T1DSHIELD-T1D: Shingrix and semaglutide for beta-cell preservationSorafenib in new-onset T1DTregs plus anti-CD20 rituximab in pediatric stage 1 T1DVerapamil to preserve residual insulin secretion in childrenAbatacept (CTLA4-Ig) to delay type 1 diabetes in at-risk relativesBANDIT: Baricitinib (JAK inhibitor) in recent-onset type 1 diabetesBARICADE-PRESERVE: Baricitinib in newly diagnosed T1DBETA PRESERVE: confirmatory teplizumab trial in recent-onset stage-3 T1DCREATE-1: CELZ-201 in recent-onset type 1 diabetesDIAGNODE-1: First intralymphatic GAD-alum dosing studyDIAGNODE-2: Intralymphatic GAD-alum (Diamyd) in recent-onset type 1 diabetesImatinib in recent-onset type 1 diabetesJAKPOT T1D: Abrocitinib and ritlecitinib in new-onset T1DLantidra (donislecel): purified allogeneic islet cell therapy (CIT-07)Low-dose anti-thymocyte globulin (ATG) ± GCSF in new-onset T1D (Haller / TrialNet)PROTECT: Teplizumab in children and adolescents with recent-onset type 1 diabetesProtégé: Anti-CD3 (teplizumab) in recent-onset type 1 diabetesRituximab-pvvr followed by abatacept in new-onset T1D (TrialNet T1D RELAY / TN25)T1DAL: Alefacept in new-onset type 1 diabetesT1GER: Golimumab in youth with new-onset type 1 diabetesTN-09: Abatacept (CTLA4-Ig) in recent-onset type 1 diabetesUST1D2: Ustekinumab phase-2/3 in adults with recent-onset T1DUSTEKID: Ustekinumab in adolescents with recent-onset type 1 diabetesVC-01: ViaCyte first-gen encapsulated stem-cell isletsVCTX210: first CRISPR-edited, device-encapsulated stem-cell islet productVerapamil to preserve beta-cell function in newly diagnosed type 1 diabetes (Ver-A-T1D)VX-264: encapsulated stem-cell islets without immunosuppressionVX-880 / zimislecel: stem-cell-derived islets (with immunosuppression)