Drug Database
AL

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

Related Research Articles

PubMedThe Egyptian journal of immunology2026-10-15

Assessment of serum levels of vitamin D and tumor necrosis factor alpha in ulcerative colitis patients at Egyptian Military Hospitals: Cross-sectional observational study.

Eldahan Wedad W, Hassan Mohamed Z H MZH, Asaad Ahmed M AM, Salaheldin Mohamed M et al.

Ulcerative colitis (UC) is a chronic inflammatory disorder confined to the colonic and rectal mucosa. The disease is marked by infiltration of immune cells, leading to excessive production of inflammatory mediators. A key pro-inflammatory cytokine that plays a vital role in the pathophysiology of ulcerative colitis is tumor necrosis factor alpha (TNF-alpha). Low levels of vitamin D have been associated with several autoimmune disorders. This study aimed to assess vitamin D serum levels in UC patients as regard TNF-alpha serum levels and the Severity of UC (UCDAI). This cross-sectional observational research was carried out at Military healthcare facilities in Cairo, Egypt, over six months, from 1 July 2025 to 31 December 2025. Utilizing a convenience sample of 50 adults aged 15 to 70 years with a confirmed diagnosis of ulcerative colitis, newly diagnosed. They were divided into two groups according to disease severity (UCDAI or Mayo score): 26 patients in the mild group & 24 patients in the moderate/severe group. Demographic data were collected from patients' interviews. Colonoscopy for ulcerative colitis disease activity index (UCDAI) score, CBC, ESR, CRP, and Fecal calprotectin (FC) were investigated at Egyptian Military hospitals. Serum levels of 25-hydroxyvitamin D (using CLIA) and TNF-alpha (using ELISA) were measured at central laboratories of the armed forces and blood bank. Correlation analysis showed Serum Vitamin D had a moderate negative correlation with UCDAI (r = -0.466, p-value= 0.001), and a strong negative correlation with serum TNF-alpha (r = -0.669, p-value <0.001). Serum TNF-alpha showed a moderate positive correlation with UCDAI (r = 0.472, p-value= 0.001). Fecal calprotectin had a strong positive correlation with UCDAI (r = 0.704, p-value <0.001) and a weak positive correlation with serum TNF-alpha (r = 0.388, p-value= 0.005). In conclusion, this study demonstrates that patients with moderate to severe ulcerative colitis had pronounced mucosal and systemic inflammation, reflected by markedly elevated fecal calprotectin and TNF-alpha levels, concomitant with significantly lower vitamin D concentrations compared with those in mild disease.

PMID 42875905
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PubMedFrontiers in aging neuroscience2026-10-15

Resting-state cortical alpha frequency in Parkinson's disease and multiple system atrophy: associations with diagnosis, age, and symptom burden.

Chen Daichao D, Tang Huada H, Pan Yanfei Y, Sang Hui H et al.

Parkinson's disease (PD) and multiple system atrophy (MSA) are clinically overlapping neurodegenerative disorders that present with a complex, heterogeneous burden of motor and non-motor symptoms. Resting-state EEG reveals that cortical alpha slowing is a hallmark of pathological aging, yet its specific presence and clinical significance in these distinct synucleinopathies remain incompletely understood. Therefore, precisely quantifying the individual alpha frequency serves as a critical, non-invasive approach to characterize cortical network dysfunction across synucleinopathies and evaluate how aging moderates its association with clinical symptom burden. We analyzed source-reconstructed resting-state EEG data from 104 participants, comprising patients with PD, patients with the parkinsonian (MSA-P) and cerebellar subtypes (MSA-C) of MSA, and healthy controls. To accurately capture oscillatory dynamics, a data-driven masking empirical mode decomposition approach was applied to extract the individual alpha frequency across canonical cortical networks. General linear models tested diagnostic group differences, age-related effects, and age-dependent associations between individual alpha frequency and clinical symptom scores. Relative to healthy controls, both PD and MSA-C exhibited significant lower cortical IAF, whereas MSA-P showed no significant global IAF difference. At the network level, significant reduction of IAF was detected in the visual and dorsal attention networks in both PD and MSA-C. Advancing age independently contributed to alpha slowing across all participants without accelerating the disease-related trajectories. Notably, chronological age significantly moderated the relationship between alpha slowing and non-motor symptoms. In older patients, reduced individual alpha frequency was strongly associated with a higher burden of overall non-motor, autonomic, and psychiatric/cognitive symptoms, a relationship not observed in younger patients or with motor symptom severity. Cortical alpha slowing was detected in PD and MSA-C, but not in MSA-P. Age independently contributes to alpha slowing and strengthens its association with non-motor symptom burden, supporting age-aware interpretation of resting-state electroencephalography biomarkers in synucleinopathies.

PMID 42876674
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PubMediScience2026-10-15

NDUFAF2 promotes abdominal aortic aneurysm formation through mitochondrial dysfunction-induced apoptosis.

He Haipeng H, Peng Jiaxin J, Chen Huining H, Zhang Yibo Y et al.

Abdominal aortic aneurysm (AAA) is a life-threatening vascular disease closely associated with mitochondrial dysfunction and apoptosis. Here, we found that NDUFAF2 (NADH dehydrogenase (ubiquinone) 1 alpha subcomplex assembly factor 2) was significantly upregulated in cultured cells and murine AAA tissues. Knockdown of NDUFAF2 in vitro attenuated Ang II-induced mitochondrial fragmentation, reactive oxygen species (ROS) production, and apoptosis in vascular smooth muscle cells (VSMCs), while improving mitochondrial membrane potential and oxygen consumption rate. In addition, NDUFAF2 knockdown reduced the expression of DRP1 (dynamin-related protein 1) while restoring the mitochondrial fusion protein OPA1 (optic atrophy 1), and OPA1 overexpression further enhanced mitochondrial integrity and function. In vivo, NDUFAF2 knockdown suppressed CaCl2-induced AAA formation, preserved aortic structure, reduced apoptosis, and restored mitochondrial complex subunits and smooth muscle cell markers. These results indicate that NDUFAF2 contributes to AAA progression by triggering mitochondrial damage and apoptosis, representing a promising therapeutic target for AAA.

PMID 42876502
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PubMedCurrent microbiology2026-10-15

Diversity and Functional Screening of Trichoderma Species from Soils in Nanchang, China.

Qiu Yanan Y, Fan Lili L, Fu Kehe K, Xiong Min M et al.

A total of 111 Trichoderma isolates were obtained from soil samples collected in Nanchang, China. Based on morphological characteristics and molecular phylogenetic analysis of the translation elongation factor 1-alpha (tef1) gene, these isolates were assigned to 16 distinct phylogenetic lineages closely related to known species, with T. semiorbis, T. asperellum, and T. koningiopsis being the most predominant, accounting for 29, 22, and 16 isolates, respectively. All isolates were functionally screened for the production of five industrially relevant enzymes (laccase, xylanase, cellulase, chitinase, and amylase) and for copper tolerance. Several strains exhibited remarkable enzymatic activities: T. asperellum TasJK96 demonstrated the highest phenol oxidase activity (1.95 ± 0.12 U·mL- 1), T. virens TviJK51 excelled in xylanase production (41.49 ± 1.02 U·mL- 1), T. afroharzianum Tafxt15 exhibited the highest cellulase activity (22.56 ± 0.70 U·mL- 1), T. lentinulae TleJK44 was the top chitinase producer (22.21 ± 0.83 U·mL- 1), and T. koningiopsis TkoJK88 demonstrated the highest amylase activity (91.26 ± 2.25 U·mL- 1). Furthermore, 13 isolates displayed tolerance to copper, with T. virens TviJK10 exhibiting growth at concentrations up to 4.90 mmol·L- 1. This study expands our understanding of Trichoderma diversity in the Nanchang region and provides a collection of promising candidate strains for future biotechnological and bioremediation applications.

PMID 42875536
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PubMedFrontiers in immunology2026-10-15

Modulation of microbiota by traditional Chinese medicine in chronic inflammatory airway disease: a systematic review and meta-analysis of animal studies.

Sai Junting J, Li Haixia H, Chun Liu L, Li Weike W et al.

A growing number of studies have indicated that traditional Chinese medicine (TCM) can regulate microbiota in chronic inflammatory airway disease (CIAD). Nevertheless, no systematic review or integrated analysis has summarized relevant evidence to date, limiting the clinical application of TCM in this field. This study followed the PRISMA reporting guidelines. We systematically searched PubMed, EMBASE, the Cochrane Library and Web of Science for animal studies published from January 1, 2006 to January 5, 2026 exploring the effects of TCM on microbiota in CIAD. Microbial diversity indices and abundance data were extracted. Meta-analysis was performed using R version 4.5.0 with the meta for package (version 5.0.1), and risk of bias was assessed using the Systematic Review Centre for Laboratory Animal Experimentation (SYRCLE) tool. A total of 25 studies published from 2016 to 2025 were included, 20 of which were enrolled into the meta-analysis. No statistically significant overall effect of TCM on the examined gut or airway alpha-diversity indices was identified after re-analysis using REML random-effects models with Hartung-Knapp adjustment. Several pooled estimates showed substantial heterogeneity and sensitivity to individual-study omission. Most included studies reported differences in beta diversity between model and TCM groups. Changes in airway and gut microbial relative abundance were heterogeneous across studies. High or unclear risk of bias was identified in most SYRCLE domains for the included studies. Current preclinical evidence suggests that TCM may be associated with changes in airway and gut microbiota in CIAD animal models. However, the updated quantitative analyses did not demonstrate statistically significant overall effects on the alpha-diversity indices examined, and evidence concerning airway microbiota and microbial relative abundance remains heterogeneous. These findings should not be interpreted as evidence of microbiota restoration or therapeutic mechanisms. Well-designed studies with more standardized methodologies are warranted to clarify the impact of TCM on lung-gut axis microecology. https://www.crd.york.ac.uk/prospero/, identifier PROSPERO CRD420261385384.

PMID 42876713
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PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-10-15

PDHA1 Hyperactivation-Mediated Glucose Metabolism Reprogramming Fuels Neutrophil NETosis and Promotes Acute Lung Injury.

Liu Yu-Biao YB, Zhong Wen-Jing WJ, Zhang Chen-Yu CY, Chen Meng-Rui MR et al.

Neutrophil extracellular trap (NET) formation, termed NETosis, is a key driver of lung tissue injury in acute lung injury/acute respiratory distress syndrome (ALI/ARDS). However, the precise mechanisms that trigger neutrophil NETosis remain incompletely understood. Here, we observed that neutrophils from both ALI mice and ARDS patients exhibited NETosis alongside a pronounced selective metabolic shift, characterized by enhanced oxidative phosphorylation (OXPHOS) and attenuated glycolytic activity. Phosphoproteomic profiling revealed that this shift was driven by aberrant activation of pyruvate dehydrogenase E1 subunit alpha (PDHA1), resulting from its dephosphorylation at Ser293. Inhibiting PDHA1 activity, using either the inhibitor 3-fluoropyruvate (3-FP) or genetic knockdown, effectively reversed this selective metabolic reprogramming and suppressed NETosis. We further constructed neutrophil-targeted 3-FP-loaded albumin nanoparticles (3-FP-BSA NPs). These nanoparticles were specifically taken up by activated neutrophils, markedly inhibited NETosis, and alleviated lipopolysaccharide-induced ALI in mice. Mechanistically, RNA-seq revealed the enrichment of the AMPK in neutrophils during NETosis. AMPK phosphorylated PDHA1 at Ser314, which disrupted the PDHA1-pyruvate dehydrogenase kinase 1 (PDK1) interaction and inhibited PDHA1 phosphorylation at Ser293. Ultimately, PDHA1 hyperactivation-driven selective metabolic reprogramming precipitated mitochondrial stress and mtROS accumulation, thereby initiating NETosis. This study defines a targetable metabolic pathway in neutrophils and advances a specific PDHA1-nanotherapeutic strategy against ALI/ARDS.

PMID 42875839
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