If you work in biologics, save this one for later.

Antibodies can do far more than stimulate the immune system. Look how adaptable they have become!

We often think of a standard monoclonal antibody as a molecule that binds a target, blocks a pathway, or recruits an immune response.

But the antibody is becoming a much broader therapeutic tool.

Change its architecture or attach a payload, and it can:
• Engage two or three targets at once
• Deliver a cytotoxic drug
• Carry a protein degrader
• Transport an oligonucleotide into a specific tissue
• Add another layer of selectivity to treatment

That is a remarkable range from one molecular scaffold.

Sure, some of these modalities are in the early days of development, but the potential is there.

The next generation of antibodies may be defined as much by what they carry and coordinate as by what they bind.

Anything else you'd add? | 16 comments on LinkedIn

Review of Vaccines for Cancer

Un post de l’ANRS MIE s’annonçant les résultats de notre étude sur la réponse à long terme de notre candidat vaccin anti VIH. Un nouvel essai est en cours de préparation et devrait débuter mi 2027

A new Nature Review from Bali Pulendran asks a fundamental question for vaccinology: Are we still defining vaccine-induced protection too narrowly?
For decades, vaccine development has relied heavily on antibody titres as correlates of protection. But human immunity is far more complex.

In this Review, Bali describes how systems vaccinology is revealing a different picture: protection emerges from integrated immune programs involving antibodies, T cells, innate immunity, baseline immune states, metabolism, the microbiome and tissue-level interactions.

Perhaps most importantly, the paper takes the discussion beyond discovery science.
If there are multiple roads to protection, how should we design clinical trials? What should count as a correlate of protection? And how can systems-level evidence eventually become useful to regulators and vaccine developers?

This is not simply about generating more omics data. It represents a potential shift from asking:
“How high is the antibody response?”
to:
“What architecture of immunity actually produces durable protection in humans?”

These are exactly the kinds of questions we hope to explore at VIF World 2027.

We are very happy to have Bali Pulendran joining us again on our SAB and, even more importantly, working with us to co-design this part of the scientific program for VIF World 2027 in Shanghai.

Looking forward to seeing where this discussion takes us.

https://lnkd.in/gUtF6_7R
#Vaccines #Immunology #SystemsVaccinology #VaccineDevelopment #VIFWorld2027

✅ 10 YEARS of RANDOMIZED TRIALS in #LUPUS ⏲️summarized on a single slide!!!! With a specific focus on phase 2(b) and 3 #RCTs, as well as whether the main endpoint was reached or not 👍 The least we can say, is that we have collectively put A LOT OF EFFORT in the development of new treatments 💊 in #SLE. As always I used only my natural intelligence (#NoAI) so please let me know if I have forgotten a trial or if something needs to be corrected.

Chimeric antigen receptor (CAR) T-cell therapy has revolutionized oncology, and its foundational logic—precise antigen recognition coupled with durable effector activity—extends naturally to chronic non-malignant diseases sustained by long-lived pathological cells. These include viral reservoirs, autoreactive B and plasma cells, activated fibroblasts, alloimmune clones, and senescent cells that remodel tissue niches and evade clearance by conventional therapies.

This review highlights how CAR-based strategies can be adapted across diverse disease settings by redirecting engineered immune responses toward disease-sustaining cellular compartments. Co-stimulatory domains such as CD28, 4-1BB, and OX40 enhance persistence and effector function; programmed cell death protein 1 (PD-1)–CD28 switch receptors reverse inhibitory signaling; and cytokine-resistant CARs incorporating dominant-negative transforming growth factor-β (TGF-β) receptors maintain activity within suppressive microenvironments.

We discuss these approaches across infections, including human immunodeficiency virus (HIV) and Epstein–Barr virus (EBV); autoimmunity involving CD19- and B-cell maturation antigen (BCMA)-directed depletion strategies and CAR-engineered regulatory T cells (CAR-Tregs); fibrosis targeting fibroblast activation protein (FAP); hemophilia using B-cell antibody receptor (BAR)-CARs against factor VIII and factor IX inhibitors; transplantation employing human leukocyte antigen (HLA)-specific CAR-Tregs; and senescence-associated pathologies targeting urokinase plasminogen activator receptor (uPAR) and natural killer group 2D ligands (NKG2DLs).

Early clinical experiences in systemic lupus erythematosus, systemic sclerosis, myositis, and multiple sclerosis, together with preclinical successes in chronic infections and fibrotic disease, demonstrate both feasibility and durable disease modification. By extending CAR-T therapy beyond oncology, these applications position programmable cellular immunotherapy as a broadly adaptable platform for eliminating persistent pathological cells, remodeling diseased tissue environments, and restoring long-term immune homeostasis.





Great review by Saurabh Upadhyay, @Sungwoo Cho, @Kirti Upmanyu & Moustafa Gabr. The excerpt above is from the author's manuscript.

The CAR-T therapy market is projected to grow from $5.76 billion in 2025 to $81.45 billion by 2035 - over 30% annual growth. The science works. Big Pharma is placing billion-dollar bets: Eli Lilly's $2.4B acquisition of Orna Therapeutics, AbbVie's $2.1B move for Capstan Therapeutics, BMS's $1.5B deal for Orbital Therapeutics - all in the last eighteen months.

So why do more than a third of industry leaders say they can't find the people to run any of it?

A shortage that isn't new, and isn't shrinking

This isn't a post-pandemic blip. BioPlan Associates has tracked hiring difficulty as a major constraint on biopharma manufacturing for over fifteen years, and the trend isn't improving: 36% of facilities can't fill process development roles, 28% struggle with downstream production, 27% lack sufficient process engineers.

Cytiva's 2025 Global Biopharma Index (1,250 leaders surveyed) sharpens the point: over a third of organisations report severe or critical shortages in cell and gene therapy specifically - clustered in process development, GMP manufacturing, quality, and regulatory affairs. Not the scientists who discover the therapy. The people who take it from lab to commercial scale.

Why it's structural, not cyclical

The industry keeps inventing job categories faster than anyone can train for them. Five years ago, "in vivo CAR-T" wasn't a hiring category. Every platform shift - in vivo delivery, allogeneic models, dual-antigen targeting - creates a new specialisation with no existing talent pool. Training pipelines can't keep pace with a two-year innovation cycle.

The result: a "barbell" labor market - simultaneous layoffs in some functions, fierce competition for specialists in others. Specialist searches now routinely take six to nine months, even at strong compensation.

Bench to Board, not just the bench

The scarcity that makes it hard to hire a GMP-experienced engineer also makes it hard to find a CMO who's actually taken a cell therapy through pivotal trials, or a regulatory lead fluent in ATMP approval pathways. Over 80% of biotech leaders expect workforce shortages to hurt their strategy over the next five years.

The $81 billion opportunity in CAR-T won't be limited by chemistry. It'll be limited by who's in the room to build it.

#CARTtherapy #CellAndGeneTherapy #OncologyTalent #BiopharmaHiring #LifeSciencesRecruitment #ExecutiveSearch #ExecruitTalentInsights

I’ve spent much of the past decade thinking about antibody-drug conjugates. The field has changed dramatically in that time: there are now 14 approved ADCs, including one (T-DXd) with tumor-agnostic, expression-based (HER2 3+) approval.

One constant theme I hear over and over is that target expression doesn’t predict response to ADCs. But I’ve always felt like that was an oversimplification of a complex problem.  I loved reading this new Cancer Cell review from Pistilli et al., which clearly explained the nuances in detail.

They highlight that target expression correlates well with benefits for some ADCs but not others, and suggest payload class or therapeutic design may be responsible. For example, for TROP-2-targeting ADCs, internalization kinetics seem to matter as much or more than the more commonly scored membrane abundance.

They also highlight emerging work on therapeutic resistance mechanisms including TOP1 mutations, upregulation of efflux pumps, target loss, and impaired internalization (e.g., EGFR-HER2 heterodimerization suppressing T-DXd uptake) that can help identify why patients may stop responding.

The review expands on the traditional four-step mechanisms (target recognition and internalization -> trafficking -> linker cleavage -> payload release) to include bystander effect and immune mediated effects. This underscores why target expression is only one of many important factors.

There’s also review of indications where there hasn’t been strong ADC activity, such as  pancreatic cancer. This could be due to a combination of antigen density, inefficient internalization, and stroma effects. Stroma modulating approaches are being explored here. 

It’s clear that matching the right ADC to the right patient will take more than a semi-quantitative IHC score. It will take a real understanding of how each individual therapeutic behaves in a given tumor environment.

If you read it, I'd love to know what you thought: https://lnkd.in/dCPw5xVs

Cancer immunotherapies have shown promise and success in a number of different types of tumours, yet many solid epithelial tumours remain recalcitrant. Somatic mutations in tumour cells can lead to the expression of neoantigens, which are potent targets of the human antitumour immune response. These can be targeted through adoptive cell transfer (ACT) of neoantigen-specific T cells, including tumour-infiltrating lymphocytes (TILs) or T cell receptor (TCR)-engineered T cells (TCR-T cells), an approach that has been shown to achieve tumour regression in patients with different types of metastatic solid tumours including melanoma, breast and gastrointestinal cancer. Immunogenomics, systems immunology and genome editing now provide multidisciplinary tools to design cell therapies against solid cancer. Here, we review historical efforts and our current conceptual understanding of ACT using TILs or TCR-T cells. Moreover, we highlight emerging correlates of response to ACT and novel strategies that integrate tumour immunology, cancer genomics, computational biology and T cell engineering for the development of next-generation cellular immunotherapies. In this Review, Krishna and colleagues draw on clinical and scientific progress in the past two decades to describe the many factors that influence clinical outcomes during adoptive cell therapy using tumour-infiltrating lymphocytes and TCR-engineered T cell therapies. They explain how T cell-intrinsic factors and tumour-specific factors in patients with advanced cancer challenge or promote the success of adoptive cell transfer (ACT), and outline new approaches in the field of ACT.

𝗡𝗲𝘅𝘁-𝗴𝗲𝗻𝗲𝗿𝗮𝘁𝗶𝗼𝗻 𝗶𝗺𝗺𝘂𝗻𝗲 𝗰𝗲𝗹𝗹 𝗲𝗻𝗴𝗮𝗴𝗲𝗿𝘀 𝗳𝗼𝗿 𝗕 𝗰𝗲𝗹𝗹 𝗱𝗲𝗽𝗹𝗲𝘁𝗶𝗼𝗻 𝗶𝗻 𝗮𝘂𝘁𝗼𝗶𝗺𝗺𝘂𝗻𝗲 𝗱𝗶𝘀𝗲𝗮𝘀𝗲𝘀

🧠 𝗔 𝗽𝗮𝗽𝗲𝗿 𝗮 𝗱𝗮𝘆 𝗸𝗲𝗲𝗽𝘀 𝗯𝗿𝗮𝗶𝗻 𝗱𝗲𝗰𝗮𝘆 𝗮𝘄𝗮𝘆 🧠
Friday, 9 October 2026

𝘐𝘮𝘮𝘶𝘯𝘦-𝘤𝘦𝘭𝘭 𝘦𝘯𝘨𝘢𝘨𝘦𝘳𝘴 (𝘐𝘊𝘌𝘴) 𝘳𝘦𝘥𝘪𝘳𝘦𝘤𝘵 𝘦𝘯𝘥𝘰𝘨𝘦𝘯𝘰𝘶𝘴 𝘪𝘮𝘮𝘶𝘯𝘦 𝘤𝘦𝘭𝘭𝘴 𝘢𝘨𝘢𝘪𝘯𝘴𝘵 𝘱𝘢𝘵𝘩𝘰𝘨𝘦𝘯𝘪𝘤 𝘉 𝘤𝘦𝘭𝘭𝘴 𝘢𝘯𝘥 𝘱𝘭𝘢𝘴𝘮𝘢 𝘤𝘦𝘭𝘭𝘴. 𝘛𝘩𝘪𝘴 𝘳𝘦𝘷𝘪𝘦𝘸 𝘦𝘹𝘱𝘭𝘰𝘳𝘦𝘴 𝘵𝘩𝘦𝘪𝘳 𝘮𝘰𝘭𝘦𝘤𝘶𝘭𝘢𝘳 𝘥𝘦𝘴𝘪𝘨𝘯, 𝘦𝘢𝘳𝘭𝘺 𝘤𝘭𝘪𝘯𝘪𝘤𝘢𝘭 𝘦𝘷𝘪𝘥𝘦𝘯𝘤𝘦 𝘢𝘯𝘥 𝘴𝘢𝘧𝘦𝘵𝘺 𝘵𝘳𝘢𝘥𝘦-𝘰𝘧𝘧𝘴.

🏗️ 𝗜𝗖𝗘 𝘀𝘁𝗿𝘂𝗰𝘁𝘂𝗿𝗲
 • Bispecifics bridge target antigens to effector receptors, forming cytotoxic immune synapses.
 • Formats span tandem antibody fragments and IgG-like molecules.
 • Fc engineering extends half-life; weaker CD3 binding limits unintended activation.

⚙️ 𝗘𝗻𝗴𝗶𝗻𝗲𝗲𝗿𝗶𝗻𝗴 𝗳𝗼𝗿 𝘀𝗮𝗳𝗲𝘁𝘆 𝗮𝗻𝗱 𝗲𝗳𝗳𝗶𝗰𝗮𝗰𝘆
 • Antigen arm: tune affinity, valency, epitope proximity and internalization.
 • Effector arm: attenuate or shield CD3 binding to limit cytokine release.
 • Pharmacokinetics: Fc or albumin binding prolongs exposure.
 • Multispecifics: combine AND/OR targeting, CD28/4-1BB co-stimulation or CD8 bias.

🎯 𝗕-𝗰𝗲𝗹𝗹 𝗮𝗻𝗱 𝗽𝗹𝗮𝘀𝗺𝗮-𝗰𝗲𝗹𝗹 𝘁𝗮𝗿𝗴𝗲𝘁𝗶𝗻𝗴
 • CD20×CD3 mosunetuzumab: lupus improvement in 4/6 patients.
 • CD19×CD3 blinatumomab: arthritis improvement in 6/6 refractory patients.
 • BCMA×CD3 teclistamab: 11/18 major responses, but 18/18 severe hypogammaglobulinaemia.

🔬 𝗦𝗲𝗹𝗲𝗰𝘁𝗶𝘃𝗲 𝗮𝘂𝘁𝗼𝗿𝗲𝗮𝗰𝘁𝗶𝘃𝗲 𝘁𝗮𝗿𝗴𝗲𝘁𝗶𝗻𝗴
 • Autoantigen×CD3 engagers eliminated anti-β2-glycoprotein I B-cell clones in vitro.
 • 9G4×CD3 selectively depleted autoreactive lupus B cells ex vivo.
 • TRBV9×CD3 and hapten-adaptor designs explore clone-selective or modular targeting.

⚔️ 𝗪𝗵𝗶𝗰𝗵 𝗰𝗲𝗹𝗹𝘀 𝗱𝗼 𝘁𝗵𝗲 𝗸𝗶𝗹𝗹𝗶𝗻𝗴?
 • Conventional T cells: CD3-driven killing, with CRS and exhaustion risks.
 • γδ T cells: recruit circulating Vδ2 or tissue-resident Vδ1 populations.
 • NK cells: CD16/NKp46 engagement; B-cell depletion demonstrated in primates.
 • Myeloid cells: CD64/CD89 engagement promotes phagocytosis.

⚖️ 𝗪𝗵𝗲𝗿𝗲 𝗱𝗼 𝗜𝗖𝗘𝘀 𝗳𝗶𝘁?
 • Monoclonal antibodies: established therapies, but Fc-dependent depletion sometimes spares tissue-resident B cells.
 • ICEs: off-the-shelf, without cell manufacturing; durable remission and long-term safety remain uncertain.
 • CAR-T: deeper tissue depletion and longer remissions so far, with more complex delivery.

❓ 𝗢𝗽𝗲𝗻 𝗾𝘂𝗲𝘀𝘁𝗶𝗼𝗻𝘀
 • How much tissue and plasma-cell depletion is enough?
 • Will CD8-biased or alternative effectors reduce toxicity?
 • Will short ICE courses match CAR-T remission durability?

🔗 𝘓𝘪𝘯𝘬 𝘵𝘰 𝘵𝘩𝘦 𝘱𝘶𝘣𝘭𝘪𝘤𝘢𝘵𝘪𝘰𝘯 𝘪𝘯 𝘤𝘰𝘮𝘮𝘦𝘯𝘵𝘴
𝘐𝘭𝘭𝘶𝘴𝘵𝘳𝘢𝘵𝘪𝘰𝘯 𝘨𝘦𝘯𝘦𝘳𝘢𝘵𝘦𝘥 𝘸𝘪𝘵𝘩 𝘈𝘐 𝘴𝘶𝘱𝘱𝘰𝘳𝘵.
𝘛𝘩𝘦 𝘰𝘱𝘪𝘯𝘪𝘰𝘯𝘴 𝘴𝘩𝘢𝘳𝘦𝘥 𝘰𝘯 𝘓𝘪𝘯𝘬𝘦𝘥𝘐𝘯 𝘢𝘳𝘦 𝘮𝘺 𝘰𝘸𝘯.

𝗛𝗼𝘄 𝗮 𝗦𝗰𝗶𝗲𝗻𝘁𝗶𝗳𝗶𝗰 𝗕𝗿𝗮𝗻𝗱 𝗞𝗲𝗲𝗽𝘀 𝗮 𝗩𝗮𝗰𝗰𝗶𝗻𝗲 𝗜𝗻𝗱𝘂𝘀𝘁𝗿𝘆 𝗔𝗹𝗶𝘃𝗲
✨ Innovation shines — even as time passes.

The global shift toward next‑generation mucosal vaccines has revealed a powerful truth:
𝗮 𝘀𝗰𝗶𝗲𝗻𝘁𝗶𝗳𝗶𝗰 𝗯𝗿𝗮𝗻𝗱 𝗶𝘀 𝗺𝗼𝗿𝗲 𝘁𝗵𝗮𝗻 𝗮 𝗽𝗿𝗼𝗱𝘂𝗰𝘁; 𝗶𝘁 𝗶𝘀 𝗮𝗻 𝗲𝗰𝗼𝘀𝘆𝘀𝘁𝗲𝗺.

The recent npj Vaccines Perspective — “Current status of intranasal and inhaled COVID‑19 vaccines” — highlights a remarkable fact:
despite dozens of global attempts, only 𝗼𝗻𝗲 𝗮𝗱𝗷𝘂𝘃𝗮𝗻𝘁𝗲𝗱 𝗽𝗿𝗼𝘁𝗲𝗶𝗻‑𝗯𝗮𝘀𝗲𝗱 𝗶𝗻𝘁𝗿𝗮𝗻𝗮𝘀𝗮𝗹 𝘃𝗮𝗰𝗰𝗶𝗻𝗲 reached emergency authorization and entered high‑impact literature.

This single achievement proves something essential:
𝗮 𝘀𝘁𝗿𝗼𝗻𝗴 𝘀𝗰𝗶𝗲𝗻𝘁𝗶𝗳𝗶𝗰 𝗶𝗱𝗲𝗮, 𝘄𝗵𝗲𝗻 𝗯𝗿𝗮𝗻𝗱𝗲𝗱 𝗽𝗿𝗼𝗽𝗲𝗿𝗹𝘆, 𝗰𝗮𝗻 𝗸𝗲𝗲𝗽 𝗮𝗻 𝗲𝗻𝘁𝗶𝗿𝗲 𝗶𝗻𝗱𝘂𝘀𝘁𝗿𝘆 𝗮𝗹𝗶𝘃𝗲.

Across Nature Reviews Immunology, Signal Transduction and Targeted Therapy, and The Lancet Infectious Diseases, one message is clear:
𝗱𝗶𝘃𝗲𝗿𝘀𝗶𝗳𝗶𝗲𝗱 𝗽𝗹𝗮𝘁𝗳𝗼𝗿𝗺𝘀, 𝗺𝘂𝗰𝗼𝘀𝗮𝗹 𝗶𝗺𝗺𝘂𝗻𝗶𝘁𝘆, 𝗮𝗻𝗱 𝗶𝗻𝗻𝗼𝘃𝗮𝘁𝗶𝘃𝗲 𝗱𝗲𝗹𝗶𝘃𝗲𝗿𝘆 𝘀𝘆𝘀𝘁𝗲𝗺𝘀 𝗮𝗿𝗲 𝘁𝗵𝗲 𝗳𝘂𝘁𝘂𝗿𝗲.

This is exactly where 𝗥𝗮𝘇𝗶 𝗖𝗼𝘃 𝗣𝗮𝗿𝘀 stands as a compelling example.

🚀 Razi Cov Pars — When Innovation Becomes Legacy

🔹 𝗚𝗹𝗼𝗯𝗮𝗹 𝗿𝗲𝗰𝗼𝗴𝗻𝗶𝘁𝗶𝗼𝗻 𝗳𝗿𝗼𝗺 𝗮 𝗻𝗮𝘁𝗶𝗼𝗻𝗮𝗹 𝗶𝗻𝗻𝗼𝘃𝗮𝘁𝗶𝗼𝗻
Its presence in high‑impact literature transforms it from a domestic achievement into a scientific reference point.

🔹 𝗔 𝗽𝗿𝗼𝗽𝗿𝗶𝗲𝘁𝗮𝗿𝘆 𝗮𝗱𝗷𝘂𝘃𝗮𝗻𝘁 𝘁𝗵𝗮𝘁 𝘀𝗶𝗴𝗻𝗮𝗹𝘀 𝘁𝗲𝗰𝗵𝗻𝗼𝗹𝗼𝗴𝗶𝗰𝗮𝗹 𝗹𝗲𝗮𝗱𝗲𝗿𝘀𝗵𝗶𝗽
The RAS‑01 oil‑in‑water adjuvant has been repeatedly cited as a novel platform — proof that innovation can emerge anywhere.

🔹 𝗔 𝗯𝗿𝗮𝗻𝗱 𝘁𝗵𝗮𝘁 𝗱𝗼𝗲𝘀𝗻’𝘁 𝗳𝗮𝗱𝗲
When a scientific brand enters peer‑reviewed literature, it becomes part of the global narrative —
and science that enters the narrative never stops shining.

🌱 A Message to Young Scientists

𝗦𝗰𝗶𝗲𝗻𝗰𝗲 𝗶𝘀 𝗮 𝗹𝗼𝗻𝗴 𝗴𝗮𝗺𝗲.
Your work may take years to mature, but when it does, it becomes part of a legacy that outlives crises, trends, and headlines.

If one idea — born in a national institute — can reach global literature and influence future vaccine platforms,
then your idea can too.

Keep building.
Keep publishing.
Keep innovating.
✨ Because real science always finds its way to the light.
Stéphane Paul Stéphanie Longet

📝 #JAMAReview: #Cancer vaccines are being evaluated for treatment and prevention across multiple malignant neoplasms as advances in tumor immunology, antigen discovery, and vaccine delivery reshape the field.

This Review discusses how vaccines can stimulate adaptive immunity against neoantigens, nonmutated tumor proteins, or tumor-derived antigens, with current approved uses in melanoma, prostate cancer, and bladder cancer.

🔗 https://ja.ma/4y1RSCU

🩻⚡ CE NE SONT PAS DEUX PATIENTS. C'EST LE MÊME, À QUELQUES SEMAINES D'INTERVALLE.

À gauche, un corps envahi. Chaque tache noire est une zone où le cancer dévore du sucre à toute vitesse.

C'est le principe du TEP-scan : on injecte un glucose radioactif 🧪, et les cellules les plus voraces s'allument. Les tumeurs, elles, sont insatiables. Elles se dessinent d'elles-mêmes. 🔥

À droite, presque plus rien. ✨
Entre les deux images, une seule intervention. On a prélevé les globules blancs du patient 🩸. On les a reprogrammés génétiquement 🧬 pour qu'ils reconnaissent enfin ce qu'ils ne voyaient pas. On les a multipliés par centaines de millions 🔢. Puis on les a réinjectés.

C'est la thérapie #CAR-T. 🚗🎯
Et ce n'est pas un médicament au sens habituel. Ça ne se dissout pas, ça ne s'élimine pas. Ce sont des cellules vivantes qui continuent de se diviser dans le corps et de chasser toutes seules. 🛡️🦠
Le patient devient son propre traitement. 💪
La médecine du futur n'est plus une promesse.

Elle est là, elle est vivante, et elle porte votre nom. 🚀
#CART #Immunothérapie #Oncologie #InnovationMédicale #Biotech #MédecineRégénérative #Cancer #RechercheMédicale #Santé #Science | 119 comments on LinkedIn

"A small study showed preliminary evidence of activity in a peptide vaccine targeting KRAS mutations in pancreatic cancer.

I’ve written about an an mRNA-based pancreatic cancer vaccine that also targets KRAS, but this is a more traditional peptide vaccine, which can be used to target specific antigens on a cancer cell.
...
There is a lot of research on vaccines being used to treat cancer, and pancreatic cancer, which is difficult to treat, is one of the top priorities.

Although this study was quite small, it has a remarkable success rate of preventing cancer in individuals who had a high success rate.

This can be an important tool in fighting pancreatic cancer, one of the more dangerous cancers."

The IBD pipeline is widening. Translation must keep up.

While conventional therapy still matters, with 5-ASA, corticosteroids and immunomodulators remain part of care, depending on disease phenotype and severity, for moderate-to-severe disease, targeted options now span:

🔹 TNF blockade
🔹 α4β7 blockade
🔹 IL-12/23 and selective IL-23 inhibition
🔹 JAK inhibition
🔹 S1P modulation

Recently:

• Tulisokibart: Merck reported positive topline Phase III induction-only results in UC. ATLAS-UC met its primary and key secondary endpoints at week 12. [1]

• Duvakitug: Phase III programmes are underway in both UC and Crohn’s disease. [2]

• Obefazimod: Abivax reported positive topline Phase III induction and maintenance results in UC. [3]

• Icotrokinra: oral IL-23R inhibition is in Phase III for UC and a Phase 2b/3 programme for Crohn’s disease. [4]

Taken together, these programmes highlight at least four active development themes:

🔸 TL1A blockade
🔸 Oral targeted mechanisms
🔸 Combination strategies
🔸 Longer-acting antibody formats

More mechanisms do not automatically solve the translational problem.

𝗧𝗵𝗲 𝗾𝘂𝗲𝘀𝘁𝗶𝗼𝗻 𝗶𝘀 𝘄𝗵𝗶𝗰𝗵 𝗺𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺 𝗳𝗶𝘁𝘀 𝘄𝗵𝗶𝗰𝗵 𝘁𝗶𝘀𝘀𝘂𝗲 𝘀𝘁𝗮𝘁𝗲, 𝗱𝗶𝘀𝗲𝗮𝘀𝗲 𝗵𝗶𝘀𝘁𝗼𝗿𝘆 𝗮𝗻𝗱 𝗽𝗮𝘁𝗶𝗲𝗻𝘁 𝗯𝗶𝗼𝗹𝗼𝗴𝘆.

At RoukenBio, our ex vivo IBD service studies fresh intestinal biopsies from Crohn’s disease, UC and non-IBD donors. Readouts can include tissue integrity and imaging, cytokines, transcriptional responses and matched blood analysis.

The aim is to add human disease context while candidate and biomarker decisions are still flexible.

👉 Learn more: https://lnkd.in/d5sADiad

𝗪𝗵𝗶𝗰𝗵 𝗽𝗶𝗽𝗲𝗹𝗶𝗻𝗲 𝗱𝗶𝗿𝗲𝗰𝘁𝗶𝗼𝗻 𝗱𝗼 𝘆𝗼𝘂 𝘁𝗵𝗶𝗻𝗸 𝘄𝗶𝗹𝗹 𝗵𝗮𝘃𝗲 𝘁𝗵𝗲 𝗴𝗿𝗲𝗮𝘁𝗲𝘀𝘁 𝗰𝗹𝗶𝗻𝗶𝗰𝗮𝗹 𝗶𝗺𝗽𝗮𝗰𝘁?


[1] Merck, 22 June 2026; ATLAS-UC, NCT06052059.
[2] Sanofi/Teva; NCT07184996 and NCT07184931.
[3] Abivax; ABTECT-1 NCT05507203, ABTECT-2 NCT05507216, Maintenance NCT05535946.
[4] Johnson & Johnson; ICONIC-UC NCT07196748, ICONIC-CD NCT07196722.

#IBD #CrohnsDisease #UlcerativeColitis

Our new study with our PhD student Franck Zekre a great pediatrician and in collaboration with a smart company in US Vaxcyte. We developed a new vaccine againt P gingivalis to prevent inflammatory dosorders

T cell engagers (TCEs) are antibody-based, bispecific or multi-specific constructs that can reprogramme T cells to eliminate target cells expressing a defined surface antigen. Originally developed for cancer therapy, TCEs are now being investigated for the treatment of autoimmune diseases, with promising initial results. The interest in using TCEs for autoimmune diseases is rapidly growing given their comparable potency with cellular therapies, combined with the advantages of biologics, including ease of manufacturing, off-the-shelf availability, better safety and more convenient delivery. Here we review the history of TCEs, focus on distinct aspects of the mechanism of action of TCEs and explain design principles. We also discuss key challenges for future TCE development in autoimmunity, including enhanced safety, high convenience and complete target cell elimination. Finally, we provide an overview of the preclinical and clinical development landscape and give an outlook on next-generation TCEs that are optimized to treat a wide variety of autoimmune diseases. T cell engagers reprogramme T cells to eliminate pathogenic cell populations and are now emerging as a promising biologic strategy for autoimmune disease. This Perspective outlines their mechanisms, design principles and development challenges, highlighting next-generation approaches to improve safety, convenience and durable target cell depletion.

𝗪𝗵𝘆 𝗦𝗼𝗺𝗲 𝗩𝗮𝗰𝗰𝗶𝗻𝗲𝘀 𝗣𝗿𝗼𝘃𝗶𝗱𝗲 𝗟𝗶𝗳𝗲𝗹𝗼𝗻𝗴 𝗣𝗿𝗼𝘁𝗲𝗰𝘁𝗶𝗼𝗻 𝗪𝗵𝗶𝗹𝗲 𝗢𝘁𝗵𝗲𝗿𝘀 𝗙𝗮𝗱𝗲, 𝗮𝗻𝗱 𝗪𝗵𝗮𝘁 𝗦𝗰𝗶𝗲𝗻𝘁𝗶𝘀𝘁𝘀 𝗔𝗿𝗲 𝗗𝗼𝗶𝗻𝗴 𝗔𝗯𝗼𝘂𝘁 𝗜𝘁
One dose of yellow fever vaccine can protect a traveler for the rest of their life. One dose of this year's influenza vaccine may lose much of its protective power within months. Both engage the very same immune system, the same B cells, the same antibody factories, the same molecular memory machinery, yet they leave behind radically different legacies of protection. This is the "memory paradox" at the heart of modern vaccinology: identical immunological hardware producing wildly divergent durability. For decades, this gap was explained mostly through clinical observation rather than mechanisms. Today, tools that let scientists watch immune memory form in real time inside human lymph nodes, combined with new methods for tracking individual B-cell lines over decades, are finally providing an evidence-based answer and a fast-growing toolkit to close the durability gap that leaves under-protected populations vulnerable to entirely preventable diseases. 

Anti-Rh immunoglobulins, such as Rhogam and similar brands, are not vaccines.

💉This warning may seem silly and outdated, but incredibly, many pregnant women at risk of Rh isoimmunization who have received anti-Rh immunoglobulin preparations (such as Rhogam) believe they are vaccines and will protect them in their current and future pregnancies, or that they simply won't need them because they will be sterilized.

💉Furthermore, they underestimate the importance of administering these preparations, and even worse, they lack access to them in hospitals and cannot afford to purchase them privately.

💉RHOGAM and similar brands do not contain any antigens, so they are not vaccines. Instead, they provide immediate passive immunity (antibodies), hence the confusion. They contain IgG immunoglobulins against the D+ antigen, which react against the erythrocytes of the fetus (Rh D+), destroying or inactivating their maternal macrophage and lymphocyte antigenic stimulation.

💉During pregnancy, after 10 weeks, small amounts of fetal blood can pass into the maternal bloodstream, potentially stimulating a maternal immune response (sensitization). This response can be more pronounced after 24 weeks of gestation and in pathological conditions (trauma, placenta previa, placenta accreta, etc.).

💉Finally, with anti-Rh immunoglobulins, perinatal complications of Rh isoimmunization, such as immune hydrops fetalis, its sequelae, as well as intrauterine and postnatal fetal death, are prevented.

Sincerely, Dr. Jaider Gómez D/Gynecologist-Obstetrician.
WhatsApp +584149712890/+584166741754.
@consultdrjaider on Instagram and Facebook.
@dr_jaider on TikTok and Instagram.

#AntiRhImmunoglobulins #Rhogam #immunehydrops #consultdrjaider #RhIsoimmunization