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

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The NF-κB pathway in inflammatory responses in preeclampsia: A systematic review and meta-analysis.

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Preeclampsia is a pregnancy-specific hypertensive disorder associated with systemic inflammation, endothelial dysfunction, and adverse maternal and fetal outcomes. The nuclear factor kappa B (NF-κB) signaling pathway has been implicated in inflammatory activation, but its role in preeclampsia remains incompletely defined. This systematic review and meta-analysis aimed to evaluate the association between NF-κB pathway activation and inflammatory responses in preeclampsia. This meta-analysis reviewed 15 peer-reviewed articles focusing on the involvement of the NF-κB pathway in preeclampsia. Quantitative assessments included changes in systolic and diastolic blood pressure and levels of key inflammatory mediators, including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta, interleukin-6 (IL-6), and NF-κB. Systolic and diastolic blood pressure were significantly elevated in patients with preeclampsia. TNF-α and NF-κB levels were also significantly increased, indicating enhanced inflammatory activation associated with the disease. In contrast, interleukin-1 beta and IL-6 levels did not differ significantly, although IL-6 showed a nonsignificant trend toward increased levels. This meta-analysis suggests that NF-κB activation, together with increased TNF-α levels, may contribute to the inflammatory pathophysiology of preeclampsia. These findings support further investigation of NF-κB-related pathways, including Sirtuin 1-mediated regulation, as potential biomarkers and therapeutic targets.

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PubMedCognitive, affective & behavioral neuroscience2026-09-19

Who is to blame? Outcome controllability and error attribution differentially shape cognitive preparation and feedback evaluation.

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Sense of agency (SoA), the experience of controlling one's actions and their consequences, is crucial for self-representation and adaptive goal-directed behavior. Much of today's cognitive work is performed through interaction with systems that are not entirely reliable or are prone to operator error. Against this background, it is of particular interest to understand how perceived outcome-controllability and attribution of action-outcome disruptions feed back into cognitive processing as states of perceived agency. In this EEG study, we manipulated performance feedback in a color-discrimination task to dissociate self-attributed from system-attributed errors. Thirty-five participants completed blocks with veridical feedback, feedback suggesting increased error rates due to impaired personal performance, and feedback indicating malfunctioning response buttons. Behavioral performance was decomposed using the EZ-diffusion model, and time-frequency analyses focused on preparatory alpha and beta oscillations and feedback-locked theta activity. Both manipulated feedback conditions led to slower responses compared to veridical feedback. Diffusion modeling revealed that general performance slowing was driven by reduced drift rates, whereas differences between self- and system-attributed errors were reflected in nondecision time. In the EEG, manipulated feedback attenuated cue-related decreases in occipital alpha and sensorimotor beta power during the cue-target interval. In addition, system- versus self-attributed errors elicited stronger feedback-related midfrontal theta responses. Our findings suggest a functional dissociation within the agency inference process, where perceived controllability regulates preparatory investment of cognitive resources on a global level, while the attribution of action-outcome discrepancies seem to modulate evaluative processing.

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Amer Ibrahiem I, El Batae Hassan H, Elshaer Yasmine A YA, Sherief Dalia Elsayed DE et al.

Anti-tumor necrosis factor-α (anti-TNF-α) agents are a cornerstone in inflammatory bowel disease (IBD) therapy, yet primary non-response remains a significant practical challenge. Leucine-rich alpha-2 glycoprotein (LRG) has been recognized as a promising marker for disease activity. This study aimed to evaluate the predictive significance of pre-treatment serum LRG for response to anti-TNF-α therapy in biologic-naïve Egyptian IBD patients. In this prospective cohort study, 100 biologic-naïve IBD adult patients (50 Crohn's disease [CD], 50 ulcerative colitis [UC]) and 100 healthy controls were enrolled. Patients received induction therapy with adalimumab or infliximab. Clinical, biochemical, and endoscopic evaluations were conducted at baseline and at week 24. Response was defined by clinical indices and endoscopic improvement, while biochemical normalization was evaluated as a secondary, supportive parameter. IBD patients had significantly elevated baseline LRG levels compared to the healthy controls (p < 0.001). Responders' baseline LRG was substantially lower than that of non-responders in both UC (26.53 vs. 34.88 µg/mL; p = 0.008) and CD (26.03 vs. 35.07 µg/mL; p = 0.006). Receiver operating characteristic analysis revealed a cut-off of > 29 µg/mL for predicting non-response, yielding sensitivities of 74.2% and 80.0% with specificities of 69.57% and 65.71% for UC and CD, respectively and negative predictive values of 85.7% for UC and 88.5% for CD. Multivariate regression confirmed baseline LRG as an independent predictor of non-response. Baseline serum LRG levels > 29 µg/mL demonstrated moderate discriminatory ability for predicting primary non-response to anti-TNF-α therapy in Egyptian IBD patients. LRG may serve as a useful adjunctive biomarker for pre-treatment risk estimation and recognizing patients who may require alternative therapeutic strategies.

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PubMedWellcome open research2026-09-19

Implementation of 7-1-7 for improving timeliness in outbreak detection and response in Thailand: A mixed-methods study on challenges in application and achievement of targets in 2024-25.

Watakulsin Peeriya P, Jitpeera Charuttaporn C, Promduangsi Pitiphon P, Yueayai Khanuengnij K et al.

Infectious disease outbreaks result in unfavourable outcomes when swift actions fail. The 7-1-7 target (detect within 7 days, notify within 1 day, respond within 7 days) was proposed to improve timeliness. Thailand piloted 7-1-7 in 2024 and scaled it up nationwide in 2025. This study aimed to quantify the 7-1-7 target achievement, identify bottlenecks and enablers, and describe challenges and solutions for applying the 7-1-7 metrics. A mixed-methods study was conducted with quantitative assessment of all events meeting the national health threat criteria during January 2024 and June 2025 for timeliness, bottlenecks and enablers for meeting the 7-1-7 target. A qualitative descriptive study with in-depth interviews of key stakeholders explored challenges and solutions for applying the 7-1-7 framework. Of the 1,435 events assessed, 15% were dangerous communicable diseases and 3% occurred in hotels. Among all the events, 50% achieved the 7-1-7 target; 85%, 73%, and 83% were detected, notified and responded to in a timely manner, respectively. The median (interquartile range) duration for detection, notification and response were 0 (0-5) days, 0 (0-2) days and 2 (0-5) days, respectively. Among events that occurred in hotels, none met the 7-1-7 target. Dangerous communicable diseases had the highest notification (95%) and response performance (99%), despite lower timely detection (71%). Key bottlenecks included delayed care-seeking and weak coordination. Key stakeholders felt that the 7-1-7 metrics was useful, but the lack of standardised data sources, disease-specific guidelines and centralised data extraction made implementation difficult. Proposed solutions focused on streamlining and decentralizing the application of 7-1-7. It is appreciable that Thailand was able to apply the 7-1-7 framework and half of the events met the 7-1-7 target. However, to better the application of 7-1-7, future work should focus on strengthening data integration and formulating disease specific guidelines.

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PubMedHealth communication2026-09-19

"They Call Us Cheaters": Exploring Stigma Management Communication Strategies During GLP-1 Medication Use.

Lazenby Braidyn B, Guidry Ashley A, Price Sarah S, Shuvo Md Sazzad Mahmud MSM et al.

As GLP-1 receptor agonist medications become more popular, conversations surrounding the medication's use are becoming increasingly more complicated. Emerging research suggests that individuals taking these medications often feel stigmatized. However, understanding how individuals manage stigma through communication is less explored. Using stigma management communication theory, the current study seeks to better understand how individuals communicatively manage stigma surrounding GLP-1 medication use. A reflexive thematic analysis of interviews with GLP-1 users (n = 34) suggests that individuals evaluate their interpretations of both their own self-stigma and the public's understanding of GLP-1 and engage in various different stigma management communication strategies in response. These strategies, while effective for stigma management, may inadvertently contribute to ongoing stigmatizing discourse surrounding GLP-1 use.

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PubMedbioRxiv : the preprint server for biology2026-09-19

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Herpes simplex virus 1 (HSV-1) infects approximately 67% of the population worldwide. It establishes lifelong reservoirs in sensory neurons and has been linked to several diseases including neuronal dysfunction. Disruption of mitochondrial homeostasis is a hallmark of HSV-1 infection, however a molecular understanding of these changes and their significance is not yet well defined. HSV-1 infection causes a UL12.5-dependent inhibition of mitochondrial biogenesis through the loss of mitochondrial DNA and mitochondrial transcription factors, PGC-1α (peroxisome proliferator-activated receptor-gamma co-activator) and TFAM (mitochondrial transcription factor). Conversely, UL12.5-independent mechanisms inhibit mitochondrial fusion by activating the OMA1 metallopeptidase that cleaves the inner mitochondrial membrane fusion protein OPA1 (optic atrophy protein 1) and by down-modulating the outer mitochondrial membrane fusion protein MFN2 (mitofusin 2). This inhibition of fusion results in a smaller mitochondrial network that clusters to perinuclear regions, likely supplying energy for viral replication and envelopment. The inner mitochondrial membrane protein TIM23 is also down-modulated during infection in a UL12.5-independent mechanism. Failure of the virus to promote these changes negatively impacts the infection. Despite these changes, mitochondria are protected from mitophagy due to the viral-induced degradation of several mitophagy adaptor proteins, whereby damaged mitochondrial components, including mitochondrial DNA, are extruded via extracellular vesicles. These mitochondrial changes still support functions necessary for HSV-1 infection. Basal cell respiration is preserved, while spare respiratory capacity and extracellular acidification rates increase, indicating glycolytic activity. Mitochondrial membrane potential is also preserved. Overall, our studies provide mechanistic insight into how HSV-1 impacts mitochondria, which could contribute to viral pathogenesis. Mitochondria are often referred to as the "powerhouse" of the cell because they are the main energy producers. Disruption of mitochondrial homeostasis is associated with multiple diseases and occurs after infection with pathogens such as HSV-1. By investigating the mechanism(s) by which HSV-1 disrupts mitochondrial homeostasis, we can better understand how HSV-1 causes pathogenesis. HSV-1 infection impacts mitochondrial homeostasis through disruption of four key processes, including: 1) inhibition of mitochondrial biogenesis and the generation of new mitochondria; 2) inhibition of mitochondrial fusion, which rescues reversibly damaged mitochondria; 3) sustaining mitochondrial fission, which removes damaged content; and 4) preventing mitophagy, which clears damaged mitochondria. UL12.5-dependent and UL12.5- independent events during HSV-1 infection disrupt mitochondrial homeostasis, redirecting mitochondrial resources towards progeny virus production. These changes cause irreversible damage to host cells, ultimately driving pathogenesis.

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