Drug Database
AS

AS0-3B (AS03B1 / AS03B)

✓ Approved

GSK · therapeutic agent

What is AS0-3B?

AS0-3B is a therapeutic agent developed by GSK. It is approved for therapeutic indications via injectable (others) or intramuscular (im) injection.

Drug Profile

Brand NamesAS03B1, AS03B
CompanyGSK
RouteInjectable (Others), Intramuscular (IM) Injection
StatusApproved
Sources: ClinicalTrials.gov, GSK

Therapeutic Indications

AS0-3B is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Surgical and medical proceduresOral appliance application✓ Approved

Related Research Articles

PubMedCrohn's & colitis 3602026-08-30

Outcomes of tofacitinib dose reduction in patients with ulcerative colitis in stable remission: a long-term follow-up of the randomized RIVETING trial.

Rubin David T DT, Panés Julian J, Torres Joana J, Kobayashi Taku T et al.

Tofacitinib is an oral Janus kinase inhibitor used for the treatment of ulcerative colitis. This study evaluated efficacy/safety of dose reduction to tofacitinib 5 mg twice daily (BID) versus remaining on 10 mg BID in patients in stable remission on 10 mg BID. RIVETING, a phase 3b/4, double-blind, randomized, parallel-group trial, enrolled patients in stable remission (≥6 months) and corticosteroid-free (≥4 weeks) who received tofacitinib 10 mg BID for ≥2 years. Efficacy was reported to month (M)30 and safety was reported throughout. One hundred and forty patients were randomized (1:1) to tofacitinib 5 or 10 mg BID; 50.0% and 62.9%, respectively, maintained modified Mayo score remission at M30. Remission rate differences at M30 between doses were generally greater in patients with a baseline endoscopic subscore of 1 versus 0, and with versus without tumor necrosis factor inhibitor (TNFi) failure. 11/14 patients who dose-escalated from 5 to 10 mg BID following relapse recaptured remission (median 4.8 months). Serious infection and herpes zoster incidence rates were numerically higher with tofacitinib 10 versus 5 mg BID; overall, adverse event rates were generally similar between doses. Patients on tofacitinib 10 mg BID generally maintained modified Mayo score remission through M30 after reduction to 5 mg BID; most patients who relapsed recaptured remission after dose-escalating back to 10 mg BID. Efficacy was more likely to be maintained following dose reduction in patients with baseline endoscopic subscore 0 versus 1, without versus with prior TNFi failure. Serious infection and herpes zoster incidence was higher with tofacitinib 10 versus 5 mg BID, consistent with known safety profile. NCT03281304.

PMID 42669025
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PubMedACS central science2026-08-29

Programmed S → N Remote Cyano Migration: A Thiocyanate-Based Entry to Cyanamides and Selective Ferroptosis Inducers.

Duan Xiyan X, Feng Wanjing W, Du Fengjiao F, Liu Can C et al.

Ferroptosis represents a promising strategy to overcome apoptosis-associated drug resistance, yet access to diverse and drug-like ferroptosis-inducing chemical space remains limited. Among potential scaffolds for populating this high-value space, cyanamide-bearing molecules are attractive but synthetically challenging due to the long-standing difficulty of constructing the N-CN bond. Here we disclose a thiocyanate-enabled cascade cyclization that leverages inexpensive, low-toxicity inorganic thiocyanate as an unconventional electrophilic CN surrogate. This transformation proceeds through a cascade sequence involving SCN installation, remote S → N cyano migration, and subsequent intramolecular thiazine annulation under mild, metal-free conditions. The resulting cyanamide 3,4-dihydro-2H-1,4-thiazines exhibited nanomolar ferroptosis-inducing potency; lead compounds 3b and 3c achieved IC50 values of 6.8 nM and 14 nM, respectively; and significantly suppressed tumor growth in a lung cancer PDX model.

PMID 42666827
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PubMedJournal of biomedical informatics2026-08-29

Evaluating teacher-supervised small medical language models for institution-constrained clinical QA.

Du Gaoyuan G, Dimitriadis Dimitrios D, Li Xueping X

To evaluate whether small language models adapted on public medical benchmarks transfer reliably to institution-constrained open-answer clinical QA, and to identify which adaptation choices-supervision format, optimization objective, and backbone-determine local answer quality and evidence coverage. We used DistilGPT2 (82M) as the primary student and Llama3 70B as the teacher. We compared four strategies: public-benchmark answer-only adaptation, public-benchmark chain-of-thought adaptation, in-domain teacher-supervised question-answer fine-tuning (QAFT), and direct preference optimization (DPO). We evaluated each strategy on cleaned public benchmarks and on an internal EHR-grounded open-answer task using token-F1, exact match, hallucinated evidence rate, and evidence coverage. We tested robustness via multi-seed reruns, a controlled DPO pair-construction ablation, a hard-negative DPO variant, and cross-backbone replication on TinyLlama 1.1B and a modern Qwen2.5-3B model. Public-benchmark adaptation did not produce stable gains in repeated-seed external evaluation. In the primary internal comparison, in-domain QAFT outperformed public-benchmark transfer (F1 0.1310 vs 0.1090). DPO did not improve answer quality uniformly; instead, it shifted models toward shorter, stricter responses with lower evidence coverage. In a controlled fixed-split three-run ablation, this shift varied with rejected-response construction. TinyLlama replication showed backbone-specific DPO effects. For institution-constrained clinical QA, in-domain teacher-supervised fine-tuning was the most reliable evaluated adaptation path. Public-benchmark transfer was not a dependable proxy for local utility in the primary internal comparison, and DPO should be interpreted as operating-point control with local validation before deployment. We propose a local evaluation protocol: adapt on the target task, validate DPO as an operating-point control, and interpret groundedness jointly with evidence coverage.

PMID 42667993
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PubMedBMC plant biology2026-08-29

Dissection of quantitative trait loci governing root system architecture under aluminium toxicity stress conditions in Brassica carinata-derived Brassica juncea introgression lines.

Goud Shrusti S, Limbalkar Omkar Maharudra OM, K K Kanaka K, Naik H J Annappa A et al.

Aluminium (Al) toxicity in acidic soils is a major constraint limiting rapeseed-mustard productivity, particularly affecting Brassica juncea cultivation in acid-prone regions. The narrow genetic base of B. juncea restricts genetic improvement for Al toxicity stress tolerance. To enhance genetic variability and introgress beneficial genomic regions, Brassica carinata-derived B. juncea introgression lines (ILs) were developed and evaluated to dissect the genetic basis of root system architecture and stress tolerance under Al toxicity conditions. Significant genetic variability was observed among the ILs for fourteen morpho-physiological traits evaluated under Al toxicity stress. Genotyping-by-sequencing generated 7,434 high-quality SNP markers, which were used to construct a high-density linkage map spanning 3,234.9 cM with an average marker interval of 2.3 cM. QTL analysis identified 24 significant QTLs, including 17 associated with root and shoot morphological traits and 7 linked to stress tolerance indices. Notable QTLs included qRV.1B.1 for root volume and qNF.3B.3 for number of forks, explaining 26.3% and 26.0% of phenotypic variation, respectively. Three QTL hotspots were detected, including a prominent region on chromosome 2B harboring QTLs for multiple stress tolerance indices. Several putative candidate genes with known roles in stress response pathways were identified within these QTL regions, including COBRA-like involved in cell wall expansion, peroxidase and cytochrome P450 associated with oxidative detoxification, and GATA, SAUR-like, zinc-knuckle, and DNA damage-inducible proteins involved in stress signalling and regulation. This study elucidates the genetic architecture of Aluminium toxicity tolerance and identifies key QTLs and putative candidate genes governing root system architecture and stress adaptation in Brassica juncea introgression lines. The results demonstrate that interspecific introgression from B. carinata generated useful variation for root traits, enabling the identification of genomic regions associated with aluminium toxicity tolerance through GBS-based QTL mapping. These findings provide valuable genomic resources and promising targets for marker-assisted breeding to develop Aluminium toxicity-tolerant cultivars suitable for acidic soil environments.

PMID 42665788
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PubMedJSES reviews, reports, and techniques2026-08-28

Fragment-specific fixation for Dubberley type 3B distal humeral coronal shear fractures using headless compression screws and 2.0-mm micro-locking plates.

Honda Yuzo Y, Nakao Koyu K, Nishi Aki A, Takita Hiroyuki H et al.

PMID 42662886
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PubMedACS omega2026-08-28

Photooxidative Molecular Rearrangement of Vouacapane Diterpenes Generates Proapoptotic Spirocaesalmins.

Hernández-Padilla Laura L, Álvarez-García Leonardo R LR, Soto-Guzmán Eva E EE, Rodríguez-García Gabriela G et al.

The photooxidative reactivity of vouacapane derivatives and their potential as apoptotic inducers are explored in the present research. We report the obtention of the new diastereomeric spiroepoxylactones (+)-(5S,6R,​8S,9S,​10R,13S​,14R,15R,​16S)-15,16-epoxy-6-hydroxy-13-spirocassan-12,16-olide (2a), (-)-(5S,​6R,8S,​9S,10R,​13R,14R,​15S,16R)-15,16-epoxy-6-hydroxy-13-spirocassan-12,16-olide (2b), (+)-(5S,​8S,9S,​10R,13S,​14R,15R,​16S)-15,16-epoxy-6-oxo-13-spirocassan-12,16-olide (3a), (-)-(5S,​8S,9S,​10R,13R,​14R,15S,​16R)-15,16-epoxy-6-oxo-13-spirocassan-12,16-olide (3b), (+)-(5R,​6R,7R,​8S,9S,​10R,13S,​14R,15R,​16S)-6-benzoyloxy-15,16-epoxy-5,7-dihydroxy-13-spirocassan-12,16-olide (4a), and (-)-(5R,​6R,7R,​8S,9S,​10R,13R,​14R,15S,​16R)-6-benzoyloxy-15,16-epoxy-5,7-dihydroxy-13-spirocassan-12,16-olide (4b) by photooxidation of 6β-hydroxyvouacapane (2), 6-oxovouacapane (3), and isovouacapenol C (4), respectively. Known spirolactones (+)-(5S,6R,8S,9S,10R,13S,14R,15R,16S)-6-acetoxy-15,16-epoxy-13-spirocassan-12,16-olide (1a) and (-)-(5S,6R,8S,9S,10R,13R,14R,15S,16R)-6-acetoxy-15,16-epoxy-13-spirocassan-12,16-olide (1b) were also obtained from 6β-acetoxyvouacapane (1). All compounds were characterized by their physical and spectroscopic properties, while their absolute configurations were established by single-crystal X-ray analysis of 2a and 3a, and computational calculations of their specific rotation values. The cytotoxicity and apoptosis induction potential of the compounds were determined in vitro using HeLa and MDA-MB-231 human cancer cell lines, in comparison with CCD-18Co normal cell lines. The results showed that rearranged compounds 1b, 2a, and 4a had the highest cytotoxic activity against HeLa cells, while for MDA-MB-231 cells, the best results were obtained with derivatives 1b, 2a, and 3b.

PMID 42662387
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