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alpha-1 antitrypsin (Alfalastin / rhAAT, GTC)

✓ Approved

rEVO Biologics · SERPINA1 · Recombinant Proteins

What is alpha-1 antitrypsin?

alpha-1 antitrypsin is a recombinant proteins developed by rEVO Biologics. It is approved for therapeutic indications via unknown.

Drug Profile

Brand NamesAlfalastin, rhAAT, GTC
CompanyrEVO Biologics
Drug ClassRecombinant Proteins
Molecular TargetSERPINA1
RouteUnknown
StatusApproved
Sources: ClinicalTrials.gov, rEVO Biologics

Mechanism of Action

Molecular Targets

alpha-1 antitrypsin acts on 1 molecular target:

SERPINA1serpin family A member 1 (PRO2275, nNIF)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

alpha-1 antitrypsin is developed for 3 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Congenital, familial and genetic disordersCongenital emphysema✓ Approved
Skin and subcutaneous tissue disordersDermatitis allergicPreclinical
Skin and subcutaneous tissue disordersDermatitis atopicPreclinical

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Association between alpha-fetoprotein elevation and recurrence in patients who achieved normalized alpha-fetoprotein after curative resection for hepatocellular carcinoma: A retrospective cohort study.

Hwang Jeong Ah JA, Lee Jisun J, Yi Kyung Sik KS, Choi Chi-Hoon CH et al.

Alpha-fetoprotein (AFP) is a cornerstone biomarker for hepatocellular carcinoma (HCC) surveillance following curative resection. Although AFP normalization generally indicates effective tumor control, subsequent AFP elevation poses a diagnostic dilemma due to its potential association with both tumor recurrence and nonneoplastic liver conditions. This study aimed to determine the factors influencing AFP elevation and to assess the role of serial AFP testing for the early detection of recurrent HCC, thereby addressing an unmet need in refining postoperative surveillance strategies. In this retrospective cohort study, 705 patients who underwent curative resection for HCC between January 2018 and March 2020 and achieved AFP normalization were analyzed. Postoperative surveillance included AFP and imaging exams, with AFP elevation defined as ≥ 20 ng/mL and normalization as AFP < 20 ng/mL post-surgery. Multivariable analysis identified factors associated with AFP elevation. Recurrence occurred in 34.6%. Independent factors associated with AFP elevation included recurrence (odds ratio [OR] = 21.9; 95% confidence interval [CI] = 7.5-64.2), preoperative AFP elevation (OR = 3.6; 95% CI = 1.7-7.6), logAFP at normalization (OR = 12.7; 95% CI = 3.5-45.7), and cirrhosis (OR = 2.2; 95% CI = 1.0-4.5). In patients without recurrence, logAFP at normalization (OR = 12.6; 95% CI = 3.7-43.4) and cirrhosis (OR = 2.2; 95% CI = 1.1-4.5) were independently associated with false positive elevation. Intrahepatic recurrence accounted for 69.2%, with lesions of ≤ 1 cm composing 88.9%. Following a preceding AFP elevation, recurrence was detected after a median of 4.8 months and within 12 months in all cases. AFP elevation during postoperative surveillance is a strong indicator of HCC recurrence. In cases where AFP elevation occurs without clear radiologic evidence of recurrence, early and frequent liver MRI (at intervals of ≤ 3 months for at least 12 months) is recommended to facilitate prompt detection of intrahepatic lesions. Moreover, clinicians should be mindful that elevated normalized AFP levels and underlying cirrhosis increase the risk of false positive elevations. These findings underscore the need for a tailored surveillance strategy to optimize the early diagnosis and management of recurrent HCC.

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PubMedAesthetic plastic surgery2026-11-11

ICAM-1 Mediates the Immunosuppressive Activity of Adipose-Derived Stem Cells in the Inflammatory Environment.

Cao Jiankun J, Wang Chuan C, Yang Zhigang Z, Chen Hui H

Adipose-derived mesenchymal stem cells have gained attention in plastic and reconstructive surgery because they are efficient immunoregulators and easily accessible with minimal invasion. However, the mechanism of their immunoregulatory role in the inflammatory environment is unclear. Adipose-derived stem cells (ASCs) and peripheral blood mononuclear cells (PBMCs) were co-cultured to confirm the immunosuppressive activity of ASCs. The effects of inflammatory cytokines on the expression of vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) in ASCs were evaluated using flow cytometry. Nuclear factor-κB (NF-κB) and molecular target of rapamycin (mTOR) signaling inhibitors were used to evaluate the mechanism of tumor necrosis factor alpha (TNF-α) stimulated upregulation of ICAM-1 in ASCs. To evaluate the effect of ICAM-1 knockdown on the immunoregulatory capacity of ASCs, PBMCs were labeled with carboxyfluorescein succinimidyl ester (CFSE), and their proliferation was analyzed using flow cytometry. ASCs inhibited PBMC proliferation. ICAM-1, and not VCAM-1, responded to pro-inflammatory cytokines and was upregulated by TNF-α in a concentration- and time-dependent manner; the NF-κB pathway inhibitor specifically blocked this increase in ICAM-1 expression. Knocking down ICAM-1 attenuated the immunosuppressive effects of ASCs on PBMC proliferation. ICAM-1, and not VCAM-1, is an inflammation sensor on ASCs and plays a key role in the immunoregulatory potential of ASCs. Pro-inflammatory TNF-α significantly increases ICAM-1 expression on ASCs in a concentration- and time-dependent manner, which is mediated by the NF-κB signaling pathway. These data may provide a theoretical basis for the clinical administration of ASCs in inflammation-related diseases in plastic and reconstructive surgery. This journal requires that authors assign a level of evidence to each submission to which Evidence-Based Medicine rankings are applicable. This excludes Review Articles, Book Reviews, and manuscripts that concern Basic Science, Animal Studies, Cadaver Studies, and Experimental Studies. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

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PubMedMedComm2026-11-11

Neutrophil Extracellular Traps: From Mechanistic Insights to Therapeutic Targeting.

Fan Hongjie H, Tong Yurui Y, Tang Bufu B, Hu Jihong J et al.

Neutrophils represent the most abundant leukocytes in circulation and serve to protect the host from infection. Paradoxically, they also contribute to cancer by releasing extracellular traps known as neutrophil extracellular traps (NETs). These structures exert opposing effects on tumors, either promoting progression or suppressing growth, depending on the specific context. However, a comprehensive framework reconciling these dual roles is lacking. NETs can be reconceptualised as multimodal signal processors within the tumor microenvironment, with a primary focus on cancer while acknowledging relevance to certain inflammatory and autoimmune conditions. NETs function through three interconnected modalities: (1) biomechanical scaffolds that remodel tissue architecture via integrin-focal adhesion kinase (FAK) mechanotransduction; (2) immunometabolic hubs that drive glycolytic reprogramming and immune suppression; and (3) signal-integration platforms that concentrate oncogenic cues for synergistic pathway activation. This systems-level perspective, orchestrated by nodes such as hypoxia-inducible factor 1-alpha and integrin-FAK, elucidates how microenvironmental inputs dictate NET phenotypic polarity. Furthermore, therapeutic implications are addressed, including biomarker-guided stratification, optimal intervention timing during the perioperative period, dormancy phase, immunotherapy combinations, and strategies to disrupt modal crosstalk while preserving essential host defence. Future priorities include resolving NET heterogeneity and developing localised delivery systems. This roadmap enhances precision targeting of NETs in oncology and other fields.

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PubMedOral health & preventive dentistry2026-11-11

Validation of the Turkish Oral Health Impact Profile-17 for Assessing Oral Health-Related Quality of Life in Endodontic Patients.

Çetinkaya Oğuz Burhan OB, Gözübüyük Betül Banu BB, Yüksekkaya İrfan İ, Gündoğar Hasan H

To evaluate the reliability and construct validity of the Turkish version of the Oral Health Impact Profile-17 (OHIP-17-TR) in patients receiving endodontic treatment. This methodological, cross-sectional validation study included 229 adult patients undergoing or having recently completed endodontic treatment. Participants completed the OHIP-17-TR questionnaire. Internal consistency was assessed using Cronbach alpha and corrected item-total correlations. Construct validity was evaluated through exploratory factor analysis (EFA). Sampling adequacy was examined using the Kaiser-Meyer-Olkin (KMO) measure and Bartlett test of sphericity. Test-retest reliability was not assessed. The OHIP-17-TR showed high internal consistency, with a Cronbach alpha of 0.894. Corrected item-total correlations ranged from 0.345 to 0.675. The KMO value was 0.882, and the Bartlett test was significant (P 0.001), indicating suitability for factor analysis. Exploratory factor analysis identified a four-factor structure explaining 51.8% of the total variance, with all items demonstrating salient factor loadings. Subscale Cronbach alpha values ranged from 0.689 to 0.862. The OHIP-17-TR demonstrated good reliability and acceptable construct validity in this sample of endodontic patients. These findings support the use of OHIP-17-TR as a brief and practical patient-reported outcome measure for assessing oral health-related quality of life in endodontic research and clinical practice.

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PubMedAnalytical chemistry2026-11-11

LNA Blocker-Enhanced Multiplex Chip-Based Digital PCR for Ultrasensitive Quantification of Liver-Specific DNA Methylation in Plasma.

Lan Yanping Y, Yang Xin X, Chen Tianbin T, Huang Haixiong H et al.

Sensitive and selective quantification of rare methylated DNA in plasma remains a major analytical challenge. For methylation targets located in CpG-sparse regions, bisulfite conversion produces only subtle sequence differences between methylated and unmethylated alleles, thereby hindering selective amplification. Here, we report a blocker-enhanced multiplex chip-based digital PCR (cdPCR) strategy for the absolute quantification of liver-specific DNA methylation in plasma. The assay incorporates Locked Nucleic Acid (LNA)-modified blockers to selectively suppress unmethylated background templates, thereby enhancing single-base mismatch discrimination after bisulfite conversion. Seven liver-specific methylation sites within TBX15 were selected and organized into two quadruplex cdPCR panels together with an internal reference gene, enabling multiplex partition-level quantification. The platform achieved a limit of detection of 1 copy/μL, a limit of quantification of 0.2% methylation fraction, and excellent linearity over 1-10,000 copies/μL. In the primary cohort and independent external cohorts comprising 815 plasma samples, the resulting methylation profiles were used to develop diagnostic models using extreme gradient boosting (XGBoost) and logistic regression. The XGBoost model distinguished hepatocellular carcinoma from cirrhosis with an AUC of 0.881 in the test set and retained strong performance in early-stage and seronegative disease, outperforming alpha-fetoprotein and des-gamma-carboxy prothrombin. Additional disease-control and pan-cancer cohorts supported the specificity of the methylation-based models. These results demonstrate that coupling LNA-mediated background suppression with chip-based digital partitioning enables selective and sensitive plasma methylation analysis and provides a practical analytical framework for low-abundance nucleic acid detection.

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Sun Changrong C, Han Fei F, Xu Wenhao W, Wang Xinliang X et al.

Immune checkpoint inhibitors (ICIs) targeting the PD-1/PD-L1 axis have established a new standard of care for non-small cell lung cancer (NSCLC); however, clinical efficacy is frequently limited by primary resistance, acquired (secondary) resistance, and immune-related adverse events. The heterogeneity of the tumor immune microenvironment (TIME) is a critical determinant of therapeutic response, a state effectively regulated by the gut microbiota via the gut-lung axis. This review systematically examines the mechanistic crosstalk between intestinal commensals and the pulmonary TIME. We first delineate how specific bacterial metabolites, such as short-chain fatty acids and indole-3-acetic acid, alongside bacterial-fungal trans-kingdom interactions, modulate innate and adaptive immune responses within the lung through epigenetic remodeling and metabolic signaling, and we map the discrete points at which these gut-derived signals converge on the intrinsic metabolic programmes of pulmonary tumor cells. Furthermore, we analyze the dual role of the microbiome as a predictive biomarker, discussing the evolution from simple taxonomic abundance profiling to complex ecological topology scores and the identification of therapeutic toxicity driven by molecular mimicry, and we examine whether pre-intervention alpha or beta diversity metrics are required for patient selection. Finally, we evaluate emerging therapeutic strategies, including next-generation probiotics, bacterial-derived extracellular vesicles, and combinational interventions that aim to overcome ICI resistance by restructuring the host-microbe ecosystem, with particular attention to acquired resistance to PD-1 blockade. We also critically appraise the barriers that currently impede clinical translation, including the inter-cohort non-reproducibility of taxonomic biomarkers, methodological heterogeneity between 16S amplicon and shotgun metagenomic profiling, and the safety and regulatory constraints on fecal microbiota transplantation in immunocompromised patients. This synthesis underscores the necessity of integrating microbiome profiling into standard oncological practice to facilitate precision immunotherapy.

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