Drug Database
SH

SH-U-454

✓ Approved

Bayer AG · Small Molecule · Small Molecule

What is SH-U-454?

SH-U-454 is a small molecule developed by Bayer AG. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

CompanyBayer AG
Drug ClassSmall Molecule, Imaging Agents
RouteInjectable (Others), Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, Bayer AG

Therapeutic Indications

SH-U-454 is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Cardiac disordersArteriosclerosis coronary artery✓ Approved

Related Research Articles

PubMedBiomedizinische Technik. Biomedical engineering2026-08-26

Three-dimensional automatic segmentation and morphometric analysis of scapula computed tomography images using Swin-U-Net transformers.

Fang Qiong Q, Liu Meimei M, Xu Jun J, Zhao Sen S et al.

To develop and validate a method based on Swin-U-Net transformers for three-dimensional (3D) automatic segmentation of scapula computed tomography (CT) images and automated measurement of scapular morphometric parameters. CT scans from 106 healthy adults were retrospectively collected. The Swin-U-Net transformers model performed 3D scapular segmentation and automatic localization of 13 anatomical landmarks. A reference coordinate system was established from these landmarks to measure glenoid version, inclination, apex angle, height, width, and lateral acromial extension (LEA). LEA variations were analyzed according to age, sex, laterality, and acromion morphology (Bigliani classification). The model achieved a Dice coefficient of 0.95 ± 0.02 and a Hausdorff distance of 2.81 ± 0.63 mm; landmark localization error averaged 1.90 ± 0.50 mm. Measured glenoid parameters closely matched manual measurements. LEA averaged 29.67 ± 0.24 mm, with larger values on the right side and in type III (hooked) acromion morphologies (p<0.05). Age and sex had no significant effect. LEA showed strong bilateral correlation (r=0.904, p<0.001). The Swin-U-Net transformers-based method enables accurate, automated 3D scapular segmentation and quantitative morphometric analysis, providing a reliable tool for anatomical research, clinical assessment, and surgical planning of the shoulder.

PMID 42644630
Read full article →
PubMedNucleic acids research2026-08-26

Genetic studies with a uracil DNA glycosylase biosensor support a role for mitochondrial UNG1 in nuclear uracil repair.

Lin Yu-Hsiu T YT, Lott Analisa M AM, Liu Xingyu X, Abdulbaki Layla L et al.

The universally conserved enzyme uracil-DNA N-glycosylase (UNG) plays a central role in maintaining genome stability. It functions as the initiating factor in uracil base excision repair (UBER) by catalyzing the removal of uracil lesions in genomic DNA, a necessary first step in restoring genome integrity after hydrolytic deamination of cytosine to uracil or misincorporation of deoxyuridine monophosphate during replication. Although methods have been developed to study UBER in vitro and in cellulo, none provide a quantitative readout of UNG activity on the chromosomal DNA of living cells. To address this gap, we created an UNG biosensor (U-report) that utilizes a modified cytosine base editor to generate a targeted genomic uracil lesion in a fluorescent reporter for C-to-U editing activity. UNG activity ablation through uracil DNA glycosylase inhibition (Ugi) or UNG-knockout results in elevated reporter fluorescence. Isoform-specific knockouts show that mitochondrial UNG1 also contributes to UBER of nuclear DNA. Our studies establish a real-time biosensor for quantification of chromosomal DNA uracil excision activity in living cells and, in support of prior studies, indicate that both UNG isoforms should be addressed in small molecule inhibitor development programs.

PMID 42644388
Read full article →
PubMedCureus2026-08-26

Association Between Combined Preoperative Alkaline Phosphatase-Lactate Dehydrogenase Status and Postoperative Outcomes After Pancreaticoduodenectomy for Periampullary Carcinoma.

Abdulla Al Mansur Md M, Uddin Mohammad Saief MS, Azom Md Abdullah-Hel MA, Ali Emran E et al.

Periampullary carcinoma is a heterogeneous group of tumours arising within 2 cm of the papilla of Vater, including pancreatic, ampullary and biliary cancers, and is most commonly treated with pancreaticoduodenectomy (PD), a complex procedure associated with substantial postoperative morbidity. The combination of alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) provides more information than either marker individually regarding hepatobiliary tumour burden and tumour metabolic activity, respectively. This study aimed to examine the association between combined ALP-LDH status and the postoperative outcome of patients with periampullary carcinoma after PD. This was a prospective, observational study in the Department of Hepatobiliary, Pancreatic and Liver Transplantation Surgery, Bangladesh Medical University, Dhaka, from December 2024 till November 2025. Thirty periampullary carcinoma patients admitted for PD were enrolled consecutively. Patients were divided into three groups: Group 1 (ALP and LDH below their respective cut-off values, n=2); Group 2 (either ALP or LDH was elevated, n=10); and Group 3 (ALP and LDH both elevated, n=18). One-way ANOVA/Kruskal-Wallis and chi-square/Fisher-Freeman-Halton exact tests were used with effect sizes to compare groups with respect to the following variables: demographic, clinical, laboratory, tumour-related, operative, and postoperative variables. Complications after surgery were classified according to the Clavien-Dindo system. The mean age was 51.70 ± 11.03 years, and baseline demographic and clinical features were similar for the three groups. Of all the pre-operative laboratory parameters, only carbohydrate antigen 19-9 (CA 19-9) was significantly different: median 26.48 U/mL in Group 1, 212.40 U/mL in Group 2 and 569.40 U/mL in Group 3 (epsilon squared = 0.208, P = 0.022); the other laboratory parameters did not show a significant difference. The sizes of the tumour, nodal status, operative time, blood loss and pancreatic fistulas were not significantly correlated with ALP-LDH status. The major complications (Clavien-Dindo grade ≥III) were increasing, but not statistically significantly, from 0% to 30.0% and 66.7% in Group 2 and Group 3, respectively. With regard to the postoperative outcomes, wound infection was the only one that was statistically significantly associated with combined ALP-LDH status (Cramer's V=0.601, P=0.004), with a rate of 0% in Group 1, 30.0% in Group 2 and 83.3% in Group 3. In this small, exploratory cohort, preoperative ALP and LDH status were associated with the preoperative CA 19-9 level and postoperative wound infection, with a non-significant trend toward increased major complications; there was no significant association with most other postoperative outcomes such as pancreatic fistula, delayed gastric emptying, and 30-day mortality. Given the limited and unevenly distributed sample, these findings should be regarded as hypothesis-generating and require validation in larger, multicentre cohorts before any clinical application.

PMID 42643880
Read full article →
PubMedArchives of pharmacal research2026-08-26

Dexmedetomidine attenuates sepsis-associated NET formation and Th17 polarization through α2-adrenergic receptor-associated regulation of hepatic HPD.

Fang Haihong H, Wang Shuang S, Ma Zhuo Z, Pei Youming Y et al.

This study investigated whether dexmedetomidine (Dex) attenuates sepsis-induced inflammation and organ injury in association with hepatic 4-hydroxyphenylpyruvate dioxygenase (HPD) regulation through α2-adrenergic receptor (α2-AR) signaling. Using an integrative approach combining in vivo and in vitro models, single-cell RNA sequencing, and 16S rRNA analysis, we found that Dex suppressed NET formation, reduced pro-inflammatory cytokines, and ameliorated liver, kidney, and lung injury in a murine cecal ligation and puncture (CLP) model. Dex decreased hepatic HPD expression, which was accompanied by reduced hepatic HIF-1α levels. Genetic experiments showed that HPD silencing phenocopied several protective effects of Dex, while HPD overexpression weakened Dex's ability to inhibit NETs and provide organ protection. Conditioned-medium experiments indicated that hepatocyte-derived soluble factors convey HPD-associated signals to neutrophils; the inhibitory activity of sh-HPD conditioned medium was heat-sensitive, enriched in the > 3 kDa fraction, and linked to reduced p47phox membrane translocation. Supplementation with 4-hydroxyphenylpyruvate partially restored neutrophil ROS generation, suggesting a role for HPD-related metabolic imbalance. Multi-omics analyses showed that Dex treatment reduced intestinal Th17 cell differentiation, increased Treg proportions, and remodeled gut microbiota composition. These microbiome changes are interpreted as supporting gut-immune remodeling rather than an independent causal factor. In summary, our findings support a hepatocyte-centered immunometabolic model in which Dex treatment is associated with α2-AR-dependent HPD regulation, altered hepatic HIF-1α levels, reduced neutrophil oxidative burst and NET formation, and attenuation of Th17 polarization and organ injury in sepsis.

PMID 42642698
Read full article →
PubMedCNS neuroscience & therapeutics2026-08-26

Intranasal Administration of an Arginine-Enriched Penetratin Peptide Confers Neuroprotection via Mitochondrial Functional Modulation in a Genetic Parkinson's Disease Model.

Chang Jui-Chih JC, Yeh Cheng-Yi CY, Liu Kai-Li KL, Chao Yi-Chun YC et al.

Mitochondrial dysfunction is a central pathogenic mechanism in Parkinson's disease (PD), particularly in genetic forms associated with respiratory chain impairment. Disease-modifying therapies capable of restoring neuronal bioenergetics while achieving non-invasive brain delivery remain lacking. This study investigated the therapeutic potential of an arginine-enriched penetratin-derived peptide (PenArg) in a genetic PD model carrying the UQCRC1 (p.Tyr314Ser) mutation. The effects of PenArg labeled with 5-FAM- or biotin were evaluated in UQCRC1 knock-in SH-SY5Y cells and mice. Mitochondrial function, neuronal survival, and apoptosis were assessed using biochemical and imaging analyses. Brain distribution was evaluated 2 h after intranasal administration, and therapeutic efficacy was examined following chronic intranasal treatment (three times weekly for six months). PenArg restored mitochondrial membrane potential, improved neuronal viability, and reduced oxidative stress-induced apoptosis in cellular models. Imaging studies demonstrated partial mitochondrial localization in vitro and in vivo. Intranasal administration significantly improved locomotor performance, preserved dopaminergic neurons in the substantia nigra (SN) and striatum, and maintained hippocampal neuronal structure. Brain distribution analysis confirmed widespread brain penetration after intranasal administration. PenArg restored ATP synthase subunit beta expression and complex III activity while reducing cytochrome c release and caspase-3 activation in SN neurons. Treatment additionally attenuated skeletal muscle atrophy, enhanced antioxidant responses, and reduced circulating pro-inflammatory cytokines. PenArg confers neuroprotection through functional modulation of mitochondrial homeostasis and produces multisystem therapeutic benefits. Intranasal administration represents a non-invasive strategy with disease-modifying potential for mitochondrial-related neurodegenerative disorders.

PMID 42644489
Read full article →
PubMedAngewandte Chemie (International ed. in English)2026-08-26

Axial Sulfur Ligation Unlocks the Rigidity of p-Block Aluminum Single-Atoms for Accelerated Oxygen Reduction.

Wang Xiaochen X, Li Mengge M, Zhang Lili L, Zhang Bing B et al.

Main-group single-atom catalysts (SACs) offer improved Fenton resistance but suffer from catalytic inertness due to rigid, delocalized s/p-bands. Herein, we report a targeted "p-band engineering" strategy to unlock the oxygen reduction reaction (ORR) activity of aluminum via an axially sulfur-coordinated architecture (AlN4-S). Theoretical and spectroscopic analyses indicate that this asymmetric S-ligation drives vertical charge polarization and shifts the spin-summed occupied Al pz-state centroid. These coupled changes rebalance oxygenated-intermediate adsorption by mitigating the overly strong Al-*OH thermodynamic sink, shifting the potential-determining step to *OOH formation with a maximum uphill free-energy change of 0.61 eV at U = 1.23 V. In situ ATR-SEIRAS and in situ DRT impedance support more facile intermediate progression and reduced charge-transfer resistance. Consequently, the engineered AlSNC catalyst delivers an ORR half-wave potential of 0.920 V. In practical zinc-air batteries, it achieves a 185.6 mW cm-2 peak power density and operation for over 1500 h under the reported cycling protocol. This work provides a framework for ligand-induced p-band modulation that combines Fenton resistance with high electrocatalytic activity.

PMID 42642845
Read full article →

+9996 more articles available with a free account

Sign up free to view all articles →

Ask about SH-U-454