Archive · 2026 · October 2026

Daily digest — 2026-10-01

2026-10-01

Six science items, from gut-restricted RXFP4 agonists and covalent GBA2 inhibitors to cereblon PROTAC prodrugs and an open DNA glycosylase screen, plus four deals and setbacks: Novo–Hengrui, AstraZeneca–Summit, Roche's emugrobart exit and Merck's Recarbrio withdrawal.

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Medicinal Chemistry

6 articles

Aryl Sulfamates Get a Systematic SAR Look as Carbonic Anhydrase IX Binders

  • Ortho- and meta-substituted aryl sulfamates were synthesized and profiled by thermal shift, enzyme inhibition and a live-cell competition assay against CA IX, the isozyme overexpressed in hypoxic solid tumors.
  • The best compounds bound CA IX with very high affinity, and X-ray structures with several isozymes identified the groups driving affinity and selectivity.
  • pH-dependent binding data indicate the deprotonated, negatively charged sulfamate nitrogen coordinates the active-site zinc.
💡 Points

CA inhibitors are dominated by sulfonamides, so a clean sulfamate SAR backed by crystal structures is useful chemotype diversification. Selectivity over the ubiquitous CA I and II is what sinks tumor-CA programs, and the co-crystals give a concrete handle on it. Live-cell competition data beat purely recombinant assays, but I'd want hypoxic-cell potency and physicochemical properties before calling these lead-like.

Structure-Affinity and Selectivity of Aryl-Sulfamates as Inhibitors of Carbonic Anhydrase IX ↗

Covalent Cyclitol Aziridines Deliver a Brain-Penetrant, Selective GBA2 Inhibitor

  • GBA2 has lacked inhibitors that separate it from GBA1 and glucosylceramide synthase; the team built a focused library of electrophilic cyclitols (epoxides, cyclic sulfates, N-alkyl aziridines) from earlier β-D-arabinofuranose activity-based probes.
  • Profiling against GBA1, GBA2, GBA3 and glucosylceramide synthase identified covalent inhibitors selective for GBA2.
  • The lead is reported as the first brain-penetrant covalent inhibitor to selectively inactivate GBA2 in vivo.
💡 Points

Turning an activity-based-probe scaffold into an in vivo tool compound is a neat path, and selectivity over GBA1 and GCS is precisely what GBA2 biology has been missing. For anyone working on sphingolipid or lysosomal storage disorders this is a usable tool. My open question is the covalent off-target profile at in vivo exposure, since aziridines are not quiet electrophiles.

β-d-Arabinofuranose-configured Cyclitol Aziridines as Selective, Brain-penetrant Covalent GBA2 Inhibitors ↗

Structure-Guided RXFP4 Agonists Stay in the Gut and Ease Constipation in Mice

  • Guided by the cryo-EM structure of RXFP4, the authors built a tetrahydroisoquinoline agonist series aimed at two hurdles: close homology to RXFP3 and the need for gut-restricted exposure.
  • Lead compound 44 was a potent agonist with strong selectivity over RXFP3 and a pharmacokinetic profile heavily skewed toward ileum over plasma.
  • Oral dosing was effective in a loperamide-induced constipation mouse model.
💡 Points

Getting a small molecule onto a peptide-GPCR whose paralog looks nearly identical is the hard part, and using the cryo-EM structure to buy RXFP3 selectivity is the right play. The gut-over-plasma skew is what I'd look at first, since a locally acting agonist sidesteps systemic liabilities. I'd still want permeability, efflux and metabolic stability data behind that ileum exposure.

Structure-Guided Discovery of Highly Selective, Gut-Restricted RXFP4 Agonists for the Treatment of Constipation ↗

Azaphilone Probe Maps Reactive Lysines Across Live Bacterial Proteomes

Covalent drugsNatural productsBioinformatics & omicsChemical biology & target ID
  • SCL-alkyne, a simplified azaphilone derived from the natural product sclerotiorin, was designed to profile lysine reactivity proteome-wide in bacteria.
  • It was highly lysine-selective in vitro and in live E. coli; most engaged sites were lysines or protein N-termini, and only a small subset of reactive lysines sat in functional regions.
  • Enrichment analysis pointed to bacterial chemotaxis as a major target pathway, which was then confirmed.
💡 Points

Covalent ligand discovery has been cysteine-centric, and lysine-directed scaffolds beyond sulfonyl fluorides and activated esters are scarce, so a natural-product-derived option is appealing. The observation that few reactive lysines are functional is a sober reminder that reactivity is cheap and function is not. As an E. coli preprint it is a starting point for covalent fragments, not a lead.

Natural product-derived azaphilones are selective scaffolds for covalent lysine liganding in live cells ↗

Three Chemoselective Routes Turn Cereblon PROTACs into Cleavable Prodrugs

  • Cereblon-recruiting PROTACs are hard to derivatize for prodrug delivery; the paper offers three orthogonal handles: triazole quaternization, tertiary-amine alkylation and a hydroxyl linker.
  • The approaches give cleavable prodrugs with tunable release kinetics, compatible with PEGylated constructs and bottlebrush prodrugs.
  • Representative examples showed controlled degrader release, in vitro anticancer activity, tumor accumulation and preliminary in vivo efficacy.
💡 Points

The real PROTAC problem is exposure rather than ternary-complex cooperativity, so a modular way to mask and release them is overdue. Chemoselectivity on a glutarimide-bearing molecule is the practical point: if it works on existing degraders without re-optimization, it is genuinely reusable. I'd check release in plasma versus tumor, and whether the masked forms avoid premature cereblon engagement.

Generalizable Strategies for the Synthesis of Cereblon-Recruiting PROTAC Prodrugs ↗

Open Screening Dataset Maps Small-Molecule Inhibitors Across Nine Human DNA Glycosylases

Hit finding & screeningBioinformatics & omics
  • A Scandinavian consortium built a high-throughput biochemical assay platform for human DNA glycosylases, the eleven enzymes that initiate base excision repair.
  • A chemogenomic library was screened against nine glycosylases with assays good enough for hit calling, yielding primary and concentration-response data and several previously unreported inhibitors.
  • All data, protocols and metadata are publicly available.
💡 Points

Glycosylases have been chemically neglected, so an open, annotated screen across nine of them is starting material a hit-finding team can mine directly. Chemogenomic libraries carry target annotations, which helps with mechanism and selectivity reads. I'd immediately cross-check the hits for assay interference and DNA-binder artifacts, since nucleic-acid enzyme screens are notorious for them.

A high-throughput screening dataset of small-molecule inhibitors across human DNA glycosylases ↗

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Industry News

4 articles

Novo Pays $300M Upfront for Hengrui's Weekly Oral GLP-1/GIP Agonist

  • Novo gets exclusive rights outside mainland China, Hong Kong, Macau and Taiwan to HRS-1596, a once-weekly oral GLP-1/GIP dual agonist, for $300M upfront and up to $2.3B in milestones plus royalties.
  • The asset is Phase 1-ready, with Chinese clearance to start trials in weight management and type 2 diabetes; closing is expected in Q4 2026.
💡 Points

Paying $300M upfront for a molecule that hasn't dosed a human outside China shows how badly Novo wants an oral follow-on while Lilly presses its lead. It also fits a pattern of buying de-risked-enough optionality from outside rather than building it, after smaller deals like Nanexa. Weekly oral bioavailability is the real technical risk, and the milestone-heavy structure shields Novo if it fails.

Novo to spend $300M upfront to license Hengrui's weekly oral weight loss drug ↗

AstraZeneca Takes a $2B Stake in Summit to Pair Ivonescimab with Its ADCs

  • AstraZeneca is buying $2B of convertible preferred stock, giving it about 12% of Summit's common stock (about 10.6% fully diluted).
  • The first combination pairs Summit's PD-1xVEGF bispecific ivonescimab with AstraZeneca's CLDN18.2-directed ADC in gastrointestinal cancers; a memorandum of understanding covers a broader program with more AstraZeneca ADCs.
💡 Points

This is AstraZeneca buying a seat rather than a pipeline: equity plus combination rights instead of an acquisition or license, keeping it close to a PD-1xVEGF class it doesn't own without paying for the asset outright. The bet is that ADC plus PD-1xVEGF combinations become a next oncology backbone, with AstraZeneca's ADC portfolio as the partner of choice. The broader MOU is non-binding, so definitive terms are the thing to watch.

AstraZeneca scales Summit's PD-1xVEGF strategy with $2B investment to fuel ADC combinations ↗

Merck Pulls Recarbrio From the U.S. Market, Leaving No Late-Stage Antibacterial Programs

  • Merck is discontinuing Recarbrio, its reserve-use antibiotic combination, in the U.S. as part of a portfolio review, and says the move is unrelated to safety or quality.
  • Approved seven years ago for hospital-acquired pneumonia and complicated urinary and abdominal infections with few options, it leaves Merck with only mature antibiotics and, per trade reports, no antibacterial programs in Phase II or later.
💡 Points

Reserve antibiotics are meant to be used sparingly, which caps sales, and a big pharma walking away from one confirms the broken economics of anti-infective launches. Small biotechs will read this as a warning, and policymakers will cite it in the case for pull incentives. The open question is whether Merck out-licenses the product or simply sunsets it.

Merck discontinues a crucial antibiotic despite concerns over superbug resistance ↗

Roche Drops Emugrobart in Obesity After Interim Futility; Chugai Takes It Back

  • Roche ended obesity development of emugrobart (GYM329), an anti-latent-myostatin sweeping antibody meant to preserve muscle alongside GLP-1 therapy, after a Phase 2 GYMINDA interim analysis made meaningful weight loss unlikely.
  • Rights revert to Chugai, which is preparing to resume development in spinal muscular atrophy and is open to out-licensing; the antibody had already missed in SMA and FSHD trials in March.
💡 Points

This dents the muscle-preservation thesis in obesity: the pitch was that myostatin blockade adds lean-mass benefit on top of incretins, and this antibody didn't deliver. Other myostatin and activin-pathway programs will face sharper partner questions about what retained lean mass means clinically. A rights return usually signals a deprioritized asset, and a Phase 3 in SMA after an earlier SMA miss looks like a long shot.

Roche drops muscle-sparing obesity antibody after flunked interim analysis ↗