2. Disease Areas
  3. Inflammation or Immune System Disease Respiratory Disease
  4. Respiratory Inflammation Pulmonary Disease
  5. Acute Lung Injury

Acute Lung Injury

Acute Lung Injury (ALI) is a severe respiratory condition characterized by acute hypoxemic respiratory failure, diffuse alveolar damage, and increased pulmonary vascular permeability, often resulting from direct lung injury (e.g., pneumonia, aspiration) or indirect insults (e.g., sepsis, trauma). It represents a spectrum of severity, with the more severe form known as Acute Respiratory Distress Syndrome (ARDS), defined by specific clinical criteria including bilateral infiltrates on chest imaging, decreased arterial oxygenation, and absence of cardiac failure. ALI is associated with significant morbidity and mortality, requiring supportive care such as mechanical ventilation and management of underlying causes.

Acute Lung Injury (26):

Cat. No. Product Name CAS No. Purity Chemical Structure
  • HY-N2593
    Isorhapontigenin 32507-66-7 99.82%
    Isorhapontigenin is an orally active dietary polyphenol. Isorhapontigenin acts as a potent antioxidant that reduces the production of reactive oxygen species (ROS). Isorhapontigenin promotes the binding of JUN to the AP-1 site on the SESN2 promoter, induces SESN2 transcription, triggers MAPK8-dependent JUN activation, and upregulates the expression of PPAR-α, PGC-1α and CPT-1A to facilitate fatty acid oxidation. Isorhapontigenin induces autophagy, apoptosis and preadipocyte differentiation; it inhibits tumor growth, cell invasion, NF-κB transcriptional activity, the PI3K/Akt signaling pathway, STAT1 phosphorylation and MMP-2 expression. Isorhapontigenin alleviates oxidative stress, inflammatory cytokine release and triglyceride accumulation; it increases intracellular ATP levels and promotes Nrf2 nuclear translocation. Isorhapontigenin improves insulin sensitivity in adipose tissue and glucose tolerance, and reduces postprandial blood glucose, insulin and free fatty acid levels. Isorhapontigenin is applicable to research on bladder cancer, liver injury, chronic obstructive pulmonary disease, acute lung injury and type 2 diabetes.
    Isorhapontigenin
  • HY-N0559
    Kirenol 52659-56-0 99.82%
    Kirenol is a diterpenoid compound, an orally active apoptosis inducer and signaling pathway regulator, with a Kd value of 5.47 μM against the target CK2. Kirenol promotes the cleavage of Bid into tBid, regulates the protein levels/phosphorylation of Bax, Bcl-2, p53 and p21, and induces caspase-independent apoptosis, S-phase cell cycle arrest, ROS accumulation and cytotoxicity in cancer cells. Kirenol activates the CK2/AKT and AMPK-mTOR-ULK1 pathways, inhibits the signaling of NF-κB, TGF-β/Smads and NLRP3 inflammasome, and regulates the GSK3β, BMP and Wnt/β-catenin pathways. Kirenol induces autophagy, mitophagy and osteoblast differentiation, promotes mitochondrial fusion, and exerts antioxidant, anti-inflammatory, antifibrotic, renoprotective, cardioprotective, neuroprotective and analgesic effects. Kirenol is applicable to research related to chronic myeloid leukemia, ischemic stroke, diabetic nephropathy, heart failure, acute lung injury and osteoporosis.
    Kirenol
  • HY-N1990
    Gypenoside XLIX 94987-08-3 99.88%
    Gypenoside XLIX is a multifunctional bioactive compound that can be isolated from Gynostemma pentaphyllum, with a Ka value of 1.58 μM for its binding to SIRT1. Gypenoside XLIX acts as a PPAR-α agonist. It inhibits the activation of TLR4-mediated NF-κB signaling pathway by activating the Sirt1/Nrf2 signaling pathway, reduces ROS accumulation, and alleviates hepatic inflammatory injury in mice with sepsis-induced liver disease. Gypenoside XLIX targets SIRT1 to block YAP-NLRP3 activation and improve sepsis-induced cardiomyopathy. Gypenoside XLIX inhibits apoptosis (Apoptosis), pyroptosis (Pyroptosis), autophagy (Autophagy), lipid peroxidation, pro-inflammatory cytokines and anti-inflammatory cytokines. Gypenoside XLIX alleviates sepsis-induced splenic injury by inhibiting inflammation and oxidative stress, and mitigates sepsis-associated encephalopathy by targeting PPAR-α. Gypenoside XLIX prevents acute kidney injury by inhibiting IGFBP7/IGF1R-mediated programmed cell death and inflammation. Gypenoside XLIX inhibits the expression and activity of vascular cell adhesion molecule-1 in cytokine-induced human endothelial cells. Gypenoside XLIX is applicable to research related to acute liver injury, lung injury, cardiomyopathy, acute splenic injury, sepsis-associated encephalopathy, acute kidney injury, atherosclerosis and chronic inflammation.
    Gypenoside XLIX
  • HY-W145486
    Calcium gluconate 299-28-5 99.86%
    Calcium gluconate is an orally effective calcium salt supplement. Calcium gluconate reduces elevated serum potassium, decreased serum calcium, and postoperative myalgia associated with succinylcholine administration. Calcium gluconate restores calcium homeostasis, skeletal integrity, bone mineralization and bone density, and maintains levels of parathyroid hormone, bone resorption markers and osteoclasts. Calcium gluconate reverses LPS (HY-D1056)-induced ERK phosphorylation, inflammatory cytokine release and acute lung injury, alleviates airway inflammatory damage and suppresses immune responses. Calcium gluconate can be used in research related to postoperative myalgia, osteoporosis/osteomalacia and acute lung injury.
    Calcium gluconate
  • HY-N6066
    Praeruptorin E 78478-28-1 99.83%
    Praeruptorin E is an orally active pyranocoumarin compound. Praeruptorin E can be isolated from the dried roots of Peucedanum praeruptorum Dunn. Praeruptorin E reduces the expression of NF-κB. Praeruptorin E upregulates the expression of PXR and CYP3A4. Praeruptorin E inhibits Th2 cytokines, TNF-α, IL6, MPO, and blocks the Ca2+ slow channel. Praeruptorin E promotes pulmonary tissue repair and relaxes porcine coronary artery strips. Praeruptorin E protects mice from lipopolysaccharide- and hydrochloric acid-induced acute lung injury. Praeruptorin E can be used in studies related to asthma and acute lung injury.
    Praeruptorin E
  • HY-183337
    ZM734 3068219-50-8
    ZM734 is an orally active and selective NLRP3 inflammasome inhibitor. ZM734 inhibits the secretion of IL-1β. ZM734 alleviates pulmonary inflammation in a mouse model of acute lung injury. ZM734 can be used for the research of inflammatory diseases such as acute lung injury.
    ZM734
  • HY-181809
    BLT1-IN-1
    BLT1-IN-1 is an orally active and selective BLT1 inhibitor with an IC50 of 8.7 nM and a Kd of 121 nM. BLT1-IN-1 exerts protective effects against acute lung injury and sepsis in in vivo models. BLT1-IN-1 can be used in research related to acute lung injury and sepsis.
    BLT1-IN-1
  • HY-179429
    NLRP3-IN-85
    NLRP3-IN-85 (compound 5d) is a potent NLRP3 inhibitor that targets mitochondria in a ΔΨm-independent manner. NLRP3-IN-85 protects mitochondria from oxidative stress and inflammation damage and suppresses key inflammatory factors (NO, TNF-α, IL-6). NLRP3-IN-85 relives acute lung injury in mice and inhibits paw edema in rats. NLRP3-IN-85 can be used for acute lung injury (ALI) research.
    NLRP3-IN-85
  • HY-N2217
    Rotundic acid 20137-37-5 99.41%
    Rotundic acid is an orally effective triterpenoid with a Kd value of 51.3 µM for PTP1B. Rotundic acid downregulates the AKT/mTOR pro-survival pathway and modulates the MAPK pathway. Rotundic acid induces cell cycle S-phase arrest, DNA damage and apoptosis; it inhibits migration, invasion, angiogenesis and proliferation of cancer cells. Rotundic acid improves leptin sensitivity, regulates gut microbiota and reduces cellular senescence. Rotundic acid can be used in research related to hepatocellular carcinoma, obesity, aging, acute lung injury and type 2 diabetes.
    Rotundic acid
  • HY-124108
    Eicosatetraynoic acid 1191-85-1 99.9%
    Eicosatetraynoic acid (ETYA) is a non-metabolizable analog of Arachidonic acid (HY-109590) and also an inhibitor of the lipoxygenase (LOX)/cyclooxygenase (COX) pathway (ID50 = 8 μM and 4 μM). Eicosatetraynoic acid acts as a suicide substrate to inhibit the production of inflammatory mediators such as leukotrienes and prostaglandins. Eicosatetraynoic acid acts directly on cell membranes and membrane proteins to exert a wide range of effects, including blocking potassium channels, increasing cell membrane fluidity, elevating intracellular calcium levels, inhibiting DNA synthesis in tumor cells, inducing differentiation of certain cells, and specifically inhibiting the assembly and replication of orthopoxviruses. Eicosatetraynoic acid alleviates acute lung injury induced by chemicals such as phosgene.
    Eicosatetraynoic acid
  • HY-N3011
    Iridin 491-74-7 99.72%
    Iridin is an orally active natural isoflavone. Iridin inhibits the PI3K/AKT and PKM2 signaling pathways, and downregulates the JAK/STAT and NF-κB pathways. Iridin induces Fas-mediated extrinsic apoptosis, G2/M cell cycle arrest, and inhibits cell proliferation. Iridin reduces inflammation, inhibits ROS production, suppresses glycolysis, and also exhibits antioxidant and antidiabetic activities. Iridin can be used in research related to gastric cancer and acute lung injury.
    Iridin
  • HY-P991400
    GSK1995057 99.09%
    GSK1995057 is a human monoclonal antibody (mAb) targeting TNFRSF1A. GSK1995057 selectively binds to TNFR1, blocks the binding of TNF-α and LT-α, and does not interfere with TNFR2 signaling. GSK1995057 inhibits the activation of NF-κB, JNK and MAPK pathways, alleviates apoptosis (apoptosis) and inflammatory responses (inhibiting IL-1β, IL-6, IL-10, TNF-α), and prevents viability loss of human nucleus pulposus cells. GSK1995057 inhibits the expression of cytokines and neutrophil adhesion molecules in human pulmonary microvascular endothelial cell monolayers, and reduces inflammatory responses and lung injury symptoms in non-human primates. GSK1995057 forms complexes with HAVH autoantibodies, thereby activating TNFR1 and triggering the release of cytokines and IL-8 in human cells. GSK1995057 can be used in research related to intervertebral disc degeneration and acute lung injury.
    GSK1995057
  • HY-P10943
    APO-15 3051946-11-0 99.45%
    APO-15 is a phosphatidylserine-binding fluorescent probe and apoptosis imaging reagent. APO-15 exhibits high chemical stability under proteolytic and oxidative conditions, enables quantification and imaging of drug-induced apoptosis in preclinical mouse models, and is applicable to fixed tissue samples and multiple in vivo administration routes (Ex = 488 nm; Em = 525 nm). APO-15 can be used in studies related to acute lung injury and breast cancer.
    APO-15
  • HY-N19847
    LYRM03 1820750-36-4
    LYRM03 is a derivative of Ubenimex (HY-B0134) and a Aminopeptidase N inhibitor. LYRM03 is isolated from Streptomyces HCCB10043. LYRM03 inhibits TLR4, MyD88, NLRP3, ASC, NF-κB and p38 MAPK, stabilizes IκB, and suppresses LPS-induced expression of iNOS and COX-2. LYRM03 reduces the levels of inflammatory cytokines and oxidative stress markers, and alleviates pulmonary edema. LYRM03 exhibits anticancer activity against breast cancer. LYRM03 has anti-inflammatory activity. LYRM03 can be used in the research of acute lung injury and breast cancer.
    LYRM03
  • HY-184027
    IDO1/TDO-IN-12 2841468-09-3
    IDO1/TDO-IN-12 is an IDO1/TDO2 inhibitor with IC50 values of 0.825 and 4.04 μM, respectively. IDO1/TDO-IN-12 interacts with the ferrous heme cofactor in IDO1 as a non-competitive tryptophan inhibitor. IDO1/TDO-IN-12 inhibits nitric oxide production in LPS (HY-D1056)-stimulated immune cells. IDO1/TDO-IN-12 relieves pulmonary edema and lung injury in LPS-induced mouse models. IDO1/TDO-IN-12 can be used for the research of acute lung injury (ALI).
    IDO1/TDO-IN-12
  • HY-182283
    sEH-IN-23
    sEH-IN-23 is a soluble epoxide hydrolase inhibitor with a IC50 of 0.8 nM against human sEH and 0.7 nM against murine sEH. sEH-IN-23 inhibits inflammatory factor production mediated by NF-κB activation, reactive oxygen species (ROS) generation, and the release of pro-inflammatory cytokines IL-1β, IL-6 and TNF-α. sEH-IN-23 exhibits anti-inflammatory activity in acute lung injury models. sEH-IN-23 can be used for the research of acute lung injury.
    sEH-IN-23
  • HY-182060
    PDE4B/D-IN-5 3064814-26-9
    PDE4B/D-IN-5 (Compound P32) is a peripherally restricted, oral active inhibitor of PDE4B and PDE4D with extremely low blood-brain barrier penetration, with IC50 values of 3.4 nM and 2.2 nM, respectively. PDE4B-IN-8 inhibits the production of TNF-α. PDE4B/D-IN-5 significantly reduces the Bax/Bcl2 ratio, and alleviates oxidative stress by decreasing MPO activity and NO levels. PDE4B/D-IN-5 exhibits anti-inflammatory, antioxidant, and anti-apoptotic activities. PDE4B/D-IN-5 can be used for the research of acute lung injury.
    PDE4B/D-IN-5
  • HY-181812
    JNK2/MKK7 PPI-IN-1
    JNK2/MKK7 PPI-IN-1 is an orally active JNK2 inhibitor with an IC50 of 0.99 μM and a Kd of 81.6 μM. JNK2/MKK7 PPI-IN-1 inhibits JNK2 kinase activity, disrupts JNK2-MKK7 protein-protein interaction, and reduces c-Jun phosphorylation. JNK2/MKK7 PPI-IN-1 inhibits LPS-induced overexpression of inflammatory cytokines IL-6 and TNF-α. JNK2/MKK7 PPI-IN-1 can be used for the research of acute lung injury.
    JNK2/MKK7 PPI-IN-1
  • HY-181676
    Anti-inflammatory agent 113
    Anti-inflammatory agent 113 (compound B5) is a Cathepsin L (CTSL) inhibitor and anti-inflammatory agent with a CTSL IC50 of 5.52 μM. Anti-inflammatory agent 113 suppresses CTSL maturation, attenuates NF-κB and p38 MAPK signaling pathway activation, and binds stably in CTSL’s active site via noncovalent interactions with Asp162, Cys25, and Glu63. Anti-inflammatory agent 113 inhibits pro-inflammatory cytokine (IL-6, IL-8) production, reduces inflammatory cell lung infiltration, and alleviates lung tissue injury. Anti-inflammatory agent 113 can be used for the research of acute lung injury.
    Anti-inflammatory agent 113
  • HY-N18091
    Tovophyllin A 40738-44-1
    Tovophyllin A is an orally active xanthonoid compound. Tovophyllin A exerts neuroprotective effects against Parkinson's disease by activating the Akt/GSK3β signaling pathway. Tovophyllin A protects mouse models of liver injury by activating Nrf2. Tovophyllin A exhibits protective anti-inflammatory activity in mouse models of acute lung injury. Tovophyllin A inhibits the activation of NF-κB and subsequent release of pro-inflammatory cytokines. Tovophyllin A reduces apoptotic cell death (Apoptosis). Tovophyllin A has antiplasmodial activity. Tovophyllin A shows cytotoxic activity against lung epithelial cancer cells and breast cancer cells. Tovophyllin A can be used in research related to Parkinson's disease, liver injury, acute lung injury, lung epithelial cancer, and breast cancer.
    Tovophyllin A