若生智能
Drug Database
AL

alpha-1 antitrypsin (Alfalastin / rhAAT, GTC)

✓ Approved

rEVO Biologics · SERPINA1 · 重组蛋白

什么是 alpha-1 antitrypsin？

alpha-1 antitrypsin 是一种重组蛋白，由rEVO Biologics研发。该药已获批，用于治疗相关适应症，给药途径：Unknown。

药物档案

商品名Alfalastin, rhAAT, GTC
公司rEVO Biologics
药物类别重组蛋白
分子靶点SERPINA1
给药途径Unknown
状态Approved
来源： ClinicalTrials.gov, rEVO Biologics

作用机制

分子靶点

alpha-1 antitrypsin 作用于 1 个分子靶点：

SERPINA1serpin family A member 1 (PRO2275, nNIF)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

alpha-1 antitrypsin 针对 3 个适应症，涉及 2 个治疗领域。

治疗领域疾病/病症分期
Congenital, familial and genetic disordersCongenital emphysema✓ Approved
Skin and subcutaneous tissue disordersDermatitis allergicPreclinical
Skin and subcutaneous tissue disordersDermatitis atopicPreclinical

相关研究文献

PubMedBulletin of experimental biology and medicine2026-07-27

The Influence of Tumor Necrosis Factor Alpha on the Permeability of Nasal Epithelial Cell Monolayer.

Abalenikhina Yu V YV, Breslavets D I DI, Mylnikov P Yu PY, Builina S G SG et al.

The effect of tumor necrosis factor alpha (TNFα) on the barrier function of the nasal epithelium (RPMI 2650 cell line) was studied in in vitro experiments. It was shown that short-term exposure to the cytokine (6 h) increased transepithelial electrical resistance and decreased paracellular permeability for mannitol, which was accompanied by elevated expression of the tight junction proteins occludin and claudin-1. Prolonged exposure (48 h) caused an opposite effect, i.e., a significant decrease in the barrier function and a decrease in the content of the studied proteins. These results indicate that the proinflammatory cytokine TNFα modulates the permeability of the nasal epithelium, which should be taken into account when developing strategies for intranasal drug delivery.

PMID 42507093
阅读全文 →
PubMedAutophagy2026-07-27

Autophagy-nitric oxide reprogramming of immune metabolism: a potential avenue for asthma therapeutic advancement.

Khan Sohrab S, Sammad Abdul A, Madjirebaye Philippe P, Husnain Naqvi Muhammad Ali Ul MAU et al.

Asthma is a complex inflammatory disease where oxidative stress and immune metabolic dysfunction coexist. As master regulators of this interface, macroautophagy/autophagy and nitric oxide (NO) signaling govern immune polarization, metabolic flux, and mitochondrial integrity. While NO functions as a redox messenger that affects both protective and pathogenic outcomes, autophagy maintains cellular homeostasis through coordinated degradation and recycling processes. These pathways come together to form a regulatory triad that controls T-cell differentiation, macrophage activation, and airway remodeling. Here, we outline the ways in which autophagy-NO interactions alter immune metabolism to fuel inflammation in asthma and investigate their potential as a combined therapeutic target. We offer a systems-level perspective of immune reprogramming by mapping important molecular nodes, including those involving MTOR, AMPK, BECN1, NOS2/iNOS, and NOS3/eNOS, and connecting them to metabolic checkpoints. Finally, as a potential avenue that can offer improved efficacy and durability in the management of asthma, we highlight translational strategies that combine autophagy modulators, NO donors or inhibitors, and metabolic regulators.Abbreviations: ASM: airway smooth muscle; COPD: chronic obstructive pulmonary disease; DC: dendritic cell; FAO: fatty acid oxidation; HIF1A/HIF-1α: hypoxia inducible factor 1 subunit alpha; L-NIL: L-N6-(1-Iminoethyl)lysine (selective NOS2 inhibitor); M1 and M2: macrophage pro-inflammatory and anti-inflammatory polarization states; NO: nitric oxide; NOS2/iNOS: nitric oxide synthase 2; NOS3/eNOS: nitric oxide synthase 3; OXPHOS: oxidative phosphorylation; PPARGC1A/PGC-1α: PPARG coactivator 1 alpha; ROS: reactive oxygen species; TGFB1/TGF-β1: transforming growth factor beta 1; Treg: regulatory T cell; TSLP: thymic stromal lymphopoietin.

PMID 42504956
阅读全文 →
PubMedPhysics in medicine and biology2026-07-27

Quantitative relationship between microdosimetric quantities and plasmid DNA damage induced by auger electrons.

Han Jieun J, Kim Seohan S, Ha Sangseok S, Sung Wonmo W

Objective.This study investigated the microdosimetric characteristics of auger electrons (AEs) and their DNA damage-related physical properties, specifically evaluating the microdosimetric quantity as a physical predictor of initial DNA damage across different radiation types.Approach.Monte Carlo simulations using OpenTOPAS were conducted to calculate the frequency-mean lineal energy (yF) and the dose-mean lineal energy (yD) in spherical water targets (radii: 10-500 nm) for monoenergetic electrons (3-15 keV). DNA damage yields were quantified using TOPAS-nBio with a linear plasmid DNA model. The correlations between microdosimetric quantities and DNA damage were analyzed not only for AEs but also for protons and alpha particles to assess the universality ofyFandyDas potential biological predictors.Main results.AEs demonstrated a pronounced site-radius dependency for bothyFandyDwithin the 10-100 nm target region. Across these biologically relevant nano-scale targets, both strand break (SB) and double-SB (DSB) yields exhibited strong power-law correlations with microdosimetric quantities (R2⩾ 0.94 foryFandR2⩾ 0.89 foryD). Low-energy electrons, protons, and alpha particles aligned along a continuous microdosimetric-damage relationship despite differences in particle identity. Specifically,yFprovided a more sensitive physical predictor thanyDfor Auger electron-induced initial DNA damage in the low-lineal-energy region below 10 keVμm-1.Significance.These findings show thatyFandyDreflect nanoscale energy-deposition patterns governing initial DNA strand-break induction. This microdosimetry-damage relationship extends to low-energy AEs as well as proton and alpha particles.

PMID 42504087
阅读全文 →
PubMedProtein & cell2026-07-27

CRISPR screening identifies GNPTAB as a noncanonical STING activator driving cellular senescence.

Yin Jian J, Gao Yizhou Y, Jing Yaobin Y, Jiang Xiaoyu X et al.

Cellular senescence is accompanied by profound lysosomal alterations, yet whether lysosome-associated factors actively drive aging remains unclear. Through a focused CRISPR/Cas9 screen in human mesenchymal progenitor cells (hMPCs), we identified N-acetylglucosamine-1-phosphotransferase subunits alpha and beta (GNPTAB), an enzyme responsible for lysosomal hydrolase targeting, as a potent regulator of cellular senescence. Genetic ablation of GNPTAB attenuated senescence, whereas its overexpression accelerated senescence. This pro-senescent function occurred independently of GNPTAB's canonical enzymatic role. Instead, GNPTAB binds to the innate immune adaptor stimulator of interferon genes (STING) via a specific interface (E1119), leading to activation of STING and its downstream TANK-binding kinase 1 (TBK1), as well as pro-inflammatory gene expression. A STING-binding-deficient GNPTAB mutant (E1119A) preserved canonical lysosomal functions but failed to induce senescence, while STING depletion abolished GNPTAB-driven senescence. Together, these findings uncover a new signaling pathway wherein GNPTAB engages STING to facilitate its activation, nominating this interface as a potential target for mitigating age-related cellular dysfunction.

PMID 42505080
阅读全文 →
PubMedPediatric pulmonology2026-07-27

Comment on "Early Life Food Desert Status Is Associated With Alpha and Gamma-Tocopherol Levels and Infant Lung Function".

Shridevi Kotina K, Doiphode Megha M, Mishra Rakhi R, Dhyani Archana A et al.

PMID 42504157
阅读全文 →
PubMedPediatric pulmonology2026-07-27

Comment on "Early Life Food Desert Status Is Associated With Alpha and Gamma Tocopherol Levels and Infant Lung Function".

Mahida Kishankumar K, Jagtap Snehal Rajendra SR

PMID 42504145
阅读全文 →

注册免费账户还可查看另外 9996 篇文献

免费注册查看全部文献 →

了解更多alpha-1 antitrypsin