Cinnamomum Migao oil (CMO), derived from Cinnamomum migao H.W. Li, is commonly used to alleviate stomachache in China, but its mechanism remains unclear. This research evaluated the protective influence of CMO against gastric ulcer (GU) in ethanol-treated rat models, using untargeted/targeted metabolomics combined with molecular biology experimental techniques to determine its mechanism. The data revealed that CMO significantly ameliorated gastric mucosal damage, reduced the ulcer index, decreased the contents of TNF-α, MDA, and IL-6, and elevated SOD and GSH levels in gastric tissues. Untargeted metabolomics analysis using UHPLC Q-Exactive Orbitrap HRMS revealed that CMO treatment for GU may primarily involve the regulation of purine metabolism. Further validation using UPLC-MS/MS quantitatively measured purine metabolite levels and assessed the impact on key enzymes in the purine metabolic pathway. It was found that CMO regulated the levels of uric acid, xanthine, AMP, IMP, adenosine, inosine, adenine, and hypoxanthine in the purine metabolism pathway of GU rats by modulating ADA, XOD, and PNP. Additionally, CMO altered Nrf2, Keap1, HO-1, NQO1, and NLRP3 expression. This investigation elucidated that CMO combats GUs by regulating purine metabolism and stimulating the Nrf2/HO-1/NLRP3 axis, thereby inhibiting oxidative stress and inflammation. These results furnished a theoretical foundation for future research on CMO and its application

Background: Honghema is a traditional Chinese medicinal material and is also widely used by ethnic minority communities in Guizhou Province, where it is commonly known as “Reib ndad gunb” and “Uab Detdend”. The botanical origins were the whole plants of Laportea bulbifera (Siebold & Zucc.) Wedd. (L. bulbifera) and Girardinia diversifolia (Link) Friis (G. diversifolia). Due to morphological similarities, Urtica mairei H. Lév. (U. mairei) was often mixed as easily confusable species in actual market circulation. However, systematic research regarding the differences in chemical composition between the two botanical origins, as well as between them and their easily confusable species remain limited. This study aimed to comprehensively characterise the chemical constituents of L. bulbifera, G. diversifolia, and U. mairei, and to identify significantly differential chemical constituents for their discrimination. Methods: Data acquisition was performed using ultra-performance liquid chromatography–mass spectrometry (UPLC-MS). Multivariate statistical analyses combined with reference standard comparison were performed to investigate the differences in chemical profiles among L. bulbifera, G. diversifolia and U. mairei, identify the key differential constituents leading to the differences, and clarify their relative abundance information. Results: A total of 133, 77, and 59 chemical constituents were identified from L. bulbifera, G. diversifolia, and U. mairei, respectively. These compounds comprised flavonoids, organic acids, carbohydrates, organonitrogen compounds, terpenoids, coumarins, lipids, steroids, and other types of compounds. Flavonoids constituted the highest proportion of the compounds in L. bulbifera, whereas organic acids were the most abundant in G. diversifolia and U. mairei. Through multivariate statistical analysis, 32 inter-group differential components between L. bulbifera and G. diversifolia, 27 between L. bulbifera and U. mairei, and 13 between G. diversifolia and U. mairei were screened and identified. The core components contributing to these differences included Baimaside, Roxburic acid, 1-Galloyl-glucose, Protocatechuic acid 3-glucoside, and Schaftoside. Venn diagram analysis revealed 20 characteristic differential constituents of L. bulbifera, mainly represented by flavonoids; 6 characteristic differential constituents of G. diversifolia, primarily comprising terpenoids and organic acids; and 4 characteristic differential constituents of U. mairei, mainly represented by carbohydrates. Conclusion: Significant differences were observed among the chemical profiles of the three plant species. The method established in this study can effectively identify the chemical compositions of Honghema and its easily confusable species, revealing the key components responsible for the variations in their chemical profiles. This study provides a basis for elucidating the material foundation of Honghema and offers an effective analytical approach and valuable reference data for distinguishing Honghema from its easily confusable species.

The purpose of this study was to critically assess acute coronary syndrome (ACS) antiplatelet therapy clinical practice guidelines (CPGs) and to compile the principal recommendations therein. We systematically searched the literature between January 1, 2015 and June 29, 2025 to retrieve CPGs pertaining to antiplatelet therapy for ACS. Each CPG that met the inclusion criteria was subjected to a methodological quality assessment based on the six domains specified by the Appraisal of Guidelines for Research and Evaluation (AGREE) II tool. The basic characteristics and proposed recommendations of each included CPG were systematically retrieved and subjected to comparative analysis. From the 8,190 records initially identified, a final set of 22 CPGs was deemed eligible for inclusion. The included CPGs achieved a mean AGREE II score of 70.3

Eravacycline is a fully synthetic, fluorinated third-generation tetracycline with broad-spectrum antibacterial activity, approved for the treatment of complicated intra-abdominal infections(cIAI). Clinical studies have demonstrated favorable safety and predictable pharmacokinetic properties, supporting its use in diverse complicated infections. With increasing application in critically ill patients and those with significant organ dysfunction, increasing attention has been directed toward the potential alterations in pharmacokinetics caused by pathophysiological changes in these populations. Such variability may influence drug exposure and treatment outcomes; however, current dosing strategies largely follow standard recommendations, and evidence supporting dose optimization in special populations remains limited. This review provides a comprehensive overview of current evidence regarding the chemical structure, antimicrobial and pharmacological properties, pharmacokinetics, pharmacokinetic/pharmacodynamic characteristics, clinical applications, population pharmacokinetics, and therapeutic drug monitoring of eravacycline, aiming to support rational clinical use and individualized dosing strategies.

BackgroundIn multiple countries, clinical guidelines recommend proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors for lowering low-density lipoprotein cholesterol (LDL-C) in individuals with atherosclerotic cardiovascular disease (ASCVD). Comprehensive comparisons of the efficacy, safety, and cost-effectiveness across different PCSK9 inhibitors remain limited, and current evidence requires updating. To address this gap, this study applies a health technology assessment framework to systematically evaluate the use of PCSK9 inhibitors in patients with ASCVD.MethodsA systematic search of PubMed, EMBASE, and the Cochrane Library was conducted from database inception to February 28, 2026 to identify randomized controlled trials (RCTs) comparing PCSK9 inhibitors with standard care (statins with or without ezetimibe) in patients with ASCVD. Both pairwise and network meta-analyses were applied to synthesize direct and indirect evidence. Trial sequential analysis (TSA) was performed to evaluate the sufficiency of the accumulated data. In addition, a Markov model was developed from the perspective of the Chinese healthcare system to assess the cost-effectiveness of PCSK9 inhibitors in ASCVD patients.ResultsIn total, 24 RCTs comprising 63,328 participants were included. The results of TSA and network meta-analysis showed that, compared with SOC, all three PCSK9 inhibitors significantly reduced LDL-C levels. No statistically significant differences were found for stroke outcomes. However, both alirocumab and evolocumab significantly reduced the risk of non-fatal myocardial infarction. None of the three PCSK9 inhibitors was associated with an increased risk of serious adverse events. Using the meta-analysis findings and data from the Chinese healthcare system, the incremental cost-effectiveness ratios (ICERs) for alirocumab, evolocumab, and inclisiran versus standard care were estimated at USD 12,791.07/QALY, USD 11,646.38/QALY, and USD 31,730.14/QALY, respectively. In a scenario analysis incorporating a 72.1% reduction in the price of inclisiran, its ICER decreased to USD 9,686.31/QALY. The one-way sensitivity analysis showed that the discount rate exerted the greatest influence on model outcomes. In the price-reduction scenario, probabilistic sensitivity analysis indicated that inclisiran had a 96.6% probability of being cost-effective at a willingness-to-pay threshold of USD 13,410/QALY.ConclusionCurrently, evolocumab demonstrates relative advantages in lipid-lowering efficacy, cardiovascular outcomes, and economic value for patients with ASCVD. Alirocumab represented a cost-effective alternative. In the scenario analysis incorporating a 72.1% reduction in the price of inclisiran, inclisiran became a potentially highly cost-effective option in the Chinese healthcare setting.

This study developed a local pharmacokinetic-pharmacodynamic (PK-PD) model for Laportea bulbifera extract (LBE) in the joint cavity of adjuvant-induced arthritis (AA) rats using microdialysis technology. A stable intra-articular microdialysis sampling system was established, and the PK behavior of LBE in the joint cavities of normal and AA rats was compared using ultra performance liquid chromatography-tandem mass spectrometry analysis. The results demonstrated that the time to peak concentration and absorption half-life of the components were shortened in AA rats, whereas the area under the concentration-time curve increased. An increase in the apparent volume of distribution and a decrease in clearance were also observed, indicating accelerated absorption, increased exposure, and prolonged retention. An integrated PK-PD model was constructed by combining these data with pharmacodynamic data for tumor necrosis factor-alpha, interleukin-6, interleukin-1β, and rheumatoid factor (RF) obtained by enzyme-linked immunosorbent assay. Based on half maximal inhibitory concentration, the inhibitory potency of the five components against the four biomarkers was ranked as follows: kaempferol-3-O-rutinoside > neochlorogenic acid > rutin > chlorogenic acid > cryptochlorogenic acid. The effect compartment model revealed a linear relationship between RF and multiple components, underscoring RF's potential role as a key therapeutic target in the joint cavity. This study represents the first systematic elucidation of the local PK-PD characteristics of LBE, providing a scientific basis for developing this Miao medicinal herb and its clinical application in rheumatoid arthritis.

Letermovir (LMV) is vital for cytomegalovirus prevention in transplant recipients, but its safety and drug-drug interactions (DDI) related adverse event (AE) risks require further investigation. This study conducted a pharmacovigilance analysis to identify novel AE signals of LMV and assess DDI-related AEs with commonly co-administered drugs. AE reports from 29 quarters, from the launch of LMV to the fourth quarter of 2024, were collected from the Food and Drug Administration Adverse Event Reporting System for analysis. Two statistical models (reporting odds ratio [ROR] method and medicines and healthcare products regulatory agency) were used to identify AEs meeting the threshold, which were then compared with LMV drug labels and designated medical event (DME) risk signals. Four models were applied to detect potential AE signals related to LMV combination use, and DDI-related AEs and DMEs were analyzed in conjunction with single-drug mining results. Finally, 54 LMV AE signals were identified, of which 4 AE signals had appeared in the LMV drug labels, namely edema (ROR = 3.69), acute heart failure (ROR = 14.48), pericardial effusion (ROR = 4.77), and atrial fibrillation (ROR = 3.61). Among the remaining new AE signals, AEs with stronger ROR values included herpetic gastritis (ROR = 23,772.49), human herpesvirus 6 encephalitis (ROR = 214.17), and acute graft-versus-host disease (aGVHD) in skin (ROR = 190.2). Eight DME signals of LMV were determined, such as hepatic failure, drug-induced liver injury, renal failure, and acute kidney injury (AKI). In the DDI analysis, 279 DDI-related AE signals meeting all four model criteria were identified. Among 28 drugs commonly co-administered with LMV, immunomodulatory agents contributed the highest proportion of signals (34.4%, 96/279), with cyclosporine associated with the most AE types (10.4%, 29/279). The most frequent AEs included aplastic anemia (4.3%), esophagitis (3.9%), and renal failure (3.6%). There was a positive AE signal difference when LMV was combined with cyclosporine or tacrolimus. When used in combination with cyclosporine, in addition to cardiac events and peripheral edema listed in the LMV drug label, DME signals such as pancytopenia, febrile neutropenia, AKI, and hepatic failure may also occur; when used in combination with tacrolimus, one needs to be alert to the occurrence of aGVHD in skin/intestine. LMV use may induce cardiac AE signals such as acute heart failure, pericardial effusion, and atrial fibrillation, and may increase the risk of herpes virus reactivation. When LMV is used in combination with drugs such as cyclosporine or tacrolimus, it may exacerbate hepatic and renal toxicity. Acute heart failure and atrial fibrillation AE signals were detected when combined with cyclosporine. Future efforts should focus on the safety of LMV in clinical practice and real-world settings, with optimized medication strategies to minimize risks and enhance therapeutic outcomes.

This study compared the differences in intestinal absorption characteristics of eleven active components in Rubus multibracteatus(RM) extract(protocatechuic acid, tiliroside, scutellarin, luteoloside, astragalin, epicatechin, catechin, xanthotoxin, p-coumaric acid, caffeic acid, and apigenin-7-O-glucuronide) between normal rats and inflammatory pain model rats using the in-vitro everted intestinal sac model. The RM extract was administered at absorption concentrations of 25.0, 50.0, and 100.0 mg·mL~(-1). The contents of the eleven components in intestinal absorption solution samples were quantified by ultra-performance liquid chromatography-tandem mass spectrometry(UPLC-MS/MS), and their cumulative absorption(Q) and absorption rate constant(K_a) were calculated to evaluate the absorption characteristics of these components in normal rats and inflammatory pain model rats. The results show that except for catechin, epicatechin, and caffeic acid, the cumulative absorption-time curves of the other eight components(protocatechuic acid, tiliroside, scutellarin, luteoloside, astragalin, xanthotoxin, p-coumaric acid, and apigenin-7-O-glucuronide) exhibit an upward trend without saturation, with correlation coefficients(R~2) all > 0.9, indicating linear absorption. However, the overall absorption of all components is not dose-dependent with increasing concentration, suggesting that their absorption mechanisms are not solely passive diffusion. In both normal and model rats, the jejunum shows the highest absorption for all components except xanthotoxin. The overall absorption of seven components(excluding protocatechuic acid, caffeic acid, apigenin-7-O-glucuronide, and luteoloside) in normal rats is better than that in model rats across all intestinal segments. These findings indicate that the pathological state of inflammatory pain alters the intestinal absorption of RM extract, and its mechanism needs further investigation.

Liver injury severely limits the clinical use of voriconazole. Clarifying the mechanism and markers of voriconazole-induced liver injury is of great significance. In this study, a quantitative systems toxicology model of voriconazole-induced liver injury was constructed through integrating the mechanism-based hepatoxic parameters generated from in vitro assays into a self-built physiologically based pharmacokinetic model. The hepatotoxic substances, main mechanism, dose correlation and markers of voriconazole-induced liver injury were determined according to liver injury incidence of simulated populations. The voriconazole-treated mice, voriconazole or voriconazole N-oxide (VNO)-treated HepG2 were used to validate the relationship of liver injury with oxidative stress and VNO. The results demonstrated that the incidence of voriconazole-induced liver injury was 17.9 %, which was dose-dependent. VNO-induced oxidative stress contributed most to liver injury, which was manifested by reactive oxygen species (ROS) accumulation and antioxidant enzymes inhibition. Liver ROS/reactive nitrogen species baseline clearance Vmax and antioxidant enzymes activities were negatively correlated to plasma liver function indicators elevation and liver adenosine triphosphate loss. We concluded that VNO-induced oxidative stress was the main cause of voriconazole-induced liver injury, and basic antioxidant capability indicators might be potential markers. This study may provide new insights for mechanism understanding and early warning of voriconazole-induced liver injury.

ObjectiveTo develop and validate a method for therapeutic drug monitoring (TDM) of pyrotinib in human plasma using two-dimensional liquid chromatography (2D-LC) system.MethodThe plasma samples were pretreated with acetonitrile for protein precipitation. The mobile phase consisted of two parts: a first-dimensional mobile phase (methanol, acetonitrile, and 65 mmol/L ammonium phosphate in a ratio of 1:3:3, V/V/V) and a second-dimensional mobile phase (acetonitrile, isopropanol, and 10 mmol/L ammonium phosphate in a ratio of 16:7:1, V/V/V). The analysis cycle time was completed within 9.50 min. The method was validated for linearity, recovery, precision, accuracy, and stability.ResultsPyrotinib demonstrated excellent linearity within the range of 10.10–810.40 ng/mL with regression equation y = 556.4044× + 462.40 (R2 = 0.9995). The relative recovery rate of plasma samples was stable and reproducible, ranging from 96.82% to 100.12%. The intra-day and inter-day precisions were ≤5.30% and ≤3.80% for pyrotinib concentrations, respectively. Stability tests confirmed that pyrotinib in plasma remained stable under the following conditions: room temperature for 8 h, 4 °C for 48 h, −20 °C for 3 weeks, three freeze-thaw cycles. This method was validated in twenty patients with advanced HER2-positive breast cancer (dose range: 240–400 mg/day) The trough and peak plasma concentrations of pyrotinib ranged from 17.75–92.56 ng/mL and 51.17–232.94 ng/mL, respectively, which demonstrated significant pharmacokinetic heterogeneity.ConclusionThe developed 2D-LC analytical method not only demonstrates good precision, accuracy, recovery, and stability, but also is simple, rapid, feasible, and practical for TDM. It can be used for the concentration monitoring of pyrotinib in clinic, providing more scientific evidence for clinical practice.

OBJECTIVE:To analyze the differential expression of inflammatory proteins in the tear fluid of patients with polypoidal choroidal vasculopathy (PCV) or neovascular age-related macular degeneration (nAMD). METHODS:A total of 19 patients with PCV, 17 patients with nAMD, and 18 normal controls (NC) aged ≥50 years were enrolled. Tear samples were collected, and the expression levels of 92 inflammatory proteins were quantified using Olink technology. Differentially expressed proteins (DEPs) among the groups were analyzed, with particular attention to consistency with previous findings from aqueous humor studies. RESULTS:Olink analysis revealed extensive DEPs among PCV, nAMD, and NC groups. Compared with NC, the PCV group exhibited significant upregulation of VEGFA, Interleukin (IL) -18, IL-1α, IL-8, IL-7, Monocyte chemotactic protein (MCP)-2, and Neurturin (NRTN), along with downregulation of Tumor necrosis factor (TNF) and IL-10. The nAMD group showed a more pronounced pro-inflammatory profile, with upregulation of VEGFA, IL-18, IL-8, IL-1α, IL-7, Fibroblast growth factor (FGF)-19, MCP-1, Matrix metalloproteinase (MMP)-10, NRTN, Stem cell factor (SCF), Osteoprotegerin (OPG), Eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1), MMP-1, MCP-2, Fms-related tyrosine kinase 3 ligand (Flt3L), Tumor Necrosis Factor - like Weak Inducer of Apoptosis (TWEAK), Caspase (CASP)-8, and Tumor necrosis factor receptor superfamily member 9 (TNFRSF9), and downregulation of IL-10 and IL-12β. Comparison between PCV and nAMD indicated that IL-12β and Hepatocyte growth factor (HGF) were specifically upregulated in PCV, whereas SCF, VEGFA, Flt3L, OPG, MCP-1, T-cell surface glycoprotein CD8α (CD8α), Cystatin D (CST5), MMP-1, TNFRSF9, Transforming growth factor-α (TGF-α), 4E-BP1, and CASP-8 were significantly downregulated in PCV relative to nAMD. Boxplot analysis confirmed that Flt3L, IL-18, IL-1α, IL-7, IL-8, MCP-1, MMP-1, OPG, SCF, and VEGFA were specifically elevated in nAMD compared with both PCV and NC groups, while IL-10 was specifically suppressed in PCV. CONCLUSIONS:Tear fluid analysis represents a feasible and noninvasive approach to investigate the pathogenesis of PCV and nAMD.

Expression of concern for ‘HDACI regulates the PI3K/Akt signaling pathway to reverse MCF-7/PTX resistance by inhibiting SET’ by Weipeng Zhang et al., RSC Adv., 2016, 6, 48072–48082, https://doi.org/10.1039/C6RA06423J

Table S1. Primer lists of qPCR; Table S2. Correlation of Transgelin 2 expression with clinicopathological parameters in breast cancer; Table S3．Correlation of Transgelin 2 mRNA expression with clinicopathological features in breast cancer by multivariate logistic regression analysis; Table S4. The identification of the peak; Table S5. The annotation of the peak; Table S6. The effects of MK-2206 on IC50 value of paclitaxel in MCF-7/PTX cells; Figure S1. Differential expression of Transgelin 2 mRNA of different clinicopathological characteristics; Figure S2. Transgelin 2 expression in breast cancer cell lines; Figure S3. Transgelin 2 has no effect on the stability of the PTEN protein; Figure S4. Schematic depiction of the mechanisms underlying Transgelin 2-mediated paclitaxel resistance, migration and invasion of breast cancer by directly interacting with PTEN and activating PI3K/Akt/GSK-3β pathway.

目的 对1例肺癌患者口服厄洛替尼发生不良反应的观察与随访,优化临床药师的用药监护和提高血药浓度监测(TDM)对患者的治疗作用.方法 结合1例肺癌患者口服盐酸厄洛替尼片(特罗凯)治疗后同时发生皮肤溃疡和角膜穿孔的严重不良反应,临床药师采用循证药学和TDM对其进行药学监护.结果 通过个体化用药调整,对发生的不良反应给予对症支持治疗,患者皮肤溃疡与角膜穿孔虽未能治愈,但疼痛明显缓解.结论 临床药师在肿瘤患者用药治疗过程中,可利用临床药学专业协助临床医师对患者的个体化治疗提供药学服务,促进临床合理用药.

A 77-year-old male patient with lung cancer developed creatine kinase (CK) 887 U/L, CK-MB 89 μg/L, and high-sensitivity troponin I (hs-TnI) 43 750.1 ng/L, and ECG showed multilead ST-segment elevation after 2 cycles of combination chemotherapy with camrelizumab. The patient did not undergo the 3rd cycle of anti-tumor treatment. Clinical pharmacists participated in consultations and assisted physicians in analyzing the patient's medication. The causality between camrelizumab and the adverse event was considered as "possible" and the patient was diagnosed as immune myocarditis grade G3, receiving intravenous injection of 1 000 mg methylprednisolone pulse therapy once daily. Clinical pharmacists assisted physicians in reviewing data and developing glucocorticoid reduction plans. The dosage was reduced to 500 mg once daily after 2 days of pulse therapy. The patient's myocardial enzymes continued to decrease after glucocorticoid reduction. After 3 days, the dosage of methylprednisolone was reduced to 40 mg by intravenous injection once every 12 hours for 7 days. The patient's hs-TnI decreased to 2 248.6 ng/L. Methylprednisolone was changed to prednisone 40 mg twice daily orally. The physician's advice for prednisone dose reduction: reduce the dosage by 10-20 mg per week, monitor myocardial enzymes every week, and when the dosage is reduced to 10 mg/d, and if the myocardial enzymes return to normal, maintain it for 1-2 weeks before discontinuation. The patient followed the doctor's advice and successfully stopped medication, and no glucocorticoid-related adverse reactions and cardiac discomfort recurred. The patient did not receive immunotherapy again.

Non-small-cell lung cancer (NSCLC) remains the most common malignant cancer. We identified 43140 advanced NSCLC patients from the SEER database to develop and validate a new prognostic model. The prognostic performance was evaluated by P value, concordance index, net reclassification index, integrated discrimination improvement, and decision curve analysis. The following variables were contained in the final prognostic model: age, sex, race, TNM stage, and grade and treatment options. Compared to the AJCC staging system, this prognostic model is conducive to the implementation of individualized clinical treatment schemes and can be an important part of the precise medical care of NSCLC tumors.

Breast cancer is the leading cause of cancer death among women. Paclitaxel, a mitotic inhibitor, is highly effective in the treatment of breast cancer. However, development of resistance to paclitaxel limits its clinical use. Identifying new compounds and new strategies that are effective against breast cancer, in particular drug-resistant cancer, is of great importance. The aim of the present study was to explore the potential of a next-generation taxoid, SB-T-121205, in modulating the proliferation, migration and invasion of paclitaxel-resistant human breast cancer cells (MCF-7/PTX) and further evaluate the underlying molecular mechanisms. The results of MTT assay showed that SB-T-121205 has much higher potency to human breast cancer cells (MCF-7/S, MCF-7/PTX and MDA-MB-453 cells) than paclitaxel, while that the non-tumorigenic human bronchial epithelial cells (BEAS-2B) were slightly less sensitive to SB-T-121205 than paclitaxel. Flow cytometry and western blot methods revealed that SB-T-121205 induced cell cycle arrest at the G2/M phase and apoptosis in MCF-7/PTX cells through accelerating mitochondrial apoptotic pathway, resulting in reduction of Bcl-2/Bax ratio, as well as elevation of caspase-3, caspase-9, and poly(ADP-ribose) polymerase (PARP) levels. Moreover, SB-T-121205 changed epithelial-mesenchymal transition (EMT) property, and suppressed migration and invasion abilities of MCF-7/PTX cells. Additionally, SB-T-121205 exerted antitumor activity by inhibiting the transgelin 2 and PI3K/Akt pathway. These findings indicate that SB-T-121205 is a potent antitumor agent that promotes apoptosis and also recedes migration/invasion abilities of MCF-7/PTX cells by restraining the activity of transgelin 2 and PI3K/Akt, as well as mitochondrial apoptotic pathway. Such results suggest a potential clinical value of SB-T-121205 in breast cancer treatment.