tnf-α-in-6

TNF-α-IN-6 is an orally efficacious, allosteric inhibitor of TNFα (K_D = 6.8 nM).

Mca-(endo-1a-Dap(Dnp))-TNF-Alpha (-5 to +6) amide (human) is a peptide used as a fluorescence resonance energy transfer (FRET) based substrate for proteolytic activity assays, with cleavage-induced changes in fluorescence intensity indicating enzymatic activity [1].

1. Linalool (Linalol), a natural compound of the essential oils, has been shown to have antinociceptive, antimicrobial, and anti-inflammatory properties. 2. Linalool was protected against LPS GalN-induced liver injury through induction of antioxidant defense via Nrf2 activating and reduction inflammatory response via NF-κB inhibition. 3. Linalool biosynthesis and accumulation might be involved in plant defense against bacterial and fungal pathogens and be associated with field resistance to citrus canker. 4. Linalool significantly increased the expression of antioxidant enzymes regulated by Nrf-2 and diminished lung tissue levels of several pro-inflammatory cytokines, including tumor necrosis factor α (TNF-α) and interleukin (IL)-6.

ABzOH is a benzoic acid derivative, similar in structure to non-steroidal anti-inflammatory drugs such as aspirin, with anti-inflammatory, anti-tumor and anti-proliferative effects. ABzOH can not only inhibit the expression of tumor necrosis factor-α (TNF-a), interleukin-1β (IL-1β), interleukin-6 (IL-6) and other pro-inflammatory cytokines, but also inhibit breast cancer, lung cancer and pancreatic cancer.

1. Schisandrol B (Besigomsin) may exert neuroprotective effects by attenuating the microglia-mediated neuroinflammatory response via inhibiting the TLR4-mediated NF-κB and MAPKs signaling pathways. 2. Schisandrol B has anti-inflammatory property, potentially result from the inhibition of COX-2, iNOS, IL-6, TNF-α and NO through the down-regulation of RIP2 and NF-κB activation. 3. Schisandrol B induces marked protective effects against hepatic and renal injury induced by CCl(4) exposure through differential regulation of the MAPK signal transduction pathway. 4. Schisandrol B significantly inhibits cell proliferation in a dose-dependent manner, due to cell cycle arrest in the G1 phase with the downregulation of cyclin D1 expression and Retinoblastoma (RB) phosphorylation.

MD2-TLR4-IN-1 is a myeloid differentiation protein 2/toll-like receptor 4 (MD2-TLR4) complex inhibitor.

Isoforskolin is derived from Coleus forskohlii and reduces the secretion of TNF-α, IL-1β, IL-6 and IL-8 in human mononuclear leukocytes. Isoforskolin can be used in studies about the treatment of Lyme arthritis.

TG6-129 is an antagonist of the EP2 receptor. TG6-129 suppresses PGE2-induced elevation of cAMP in cells expressing EP2 with an IC50 value of 1.6 µM. TG6-129 reduces the expression of COX-2, IL-1β, IL-6, IL-12, IL-23 and TNF-α induced by the EP2-selective

JTE-607 is a cytokine production inhibitor. JTE-607 induces apoptosis accompanied by an increase in p21waf1 cip1 in acute myelogenous leukemia cells.

Interphotoreceptor retinoid-binding protein (651-670) (IRBP651-670), a peptide fragment of retinoid-binding protein 3 (also known as IRBP), plays a crucial role in the visual cycle by facilitating the transport of retinol and retinal between photoreceptor cells and the retinal pigment epithelium. This transport is essential for the regeneration of pigments necessary for vision. When administered at a dose of 300 µg/animal, IRBP651-670 induces autoimmune uveoretinitis in C57BL/6 mice, a model possessing the H-2b haplotype. This immunization leads to increased levels of ocular cytokines including IL-1β, IL-6, IL-17, TNF-α, and IFN-γ, promotes immune cell infiltration into the eye, and results in photoreceptor cell damage.

α-Melanocyte-stimulating hormone (α-MSH) is a 13-amino acid peptide hormone produced by post-translational processing of proopiomelanocortin (POMC) in the pituitary gland, as well as in keratinocytes, astrocytes, monocytes, and gastrointestinal cells.1It is an agonist of melanocortin receptor 3 (MC3R) and MC4R that induces cAMP production in Hepa cells expressing the human receptors (EC50s = 0.16 and 56 nM, respectively).2α-MSH (100 pM) reducesS. aureuscolony formation andC. albicansgerm tube formationin vitro.3It inhibits endotoxin-, ceramide-, TNF-α-, or okadaic acid-induced activation of NF-κB in U937 cells.1α-MSH reduces IL-6- or TNF-α-induced ear edema in mice.4It also prevents the development of adjuvant-induced arthritis in rats and increases survival in a mouse model of septic shock. Increased plasma levels of α-MSH are positively correlated with delayed disease progression and reduced death in patients with HIV.1 1.Catania, A., Airaghi, L., Colombo, G., et al.α-melanocyte-stimulating hormone in normal human physiology and disease statesTrends Endocrinol. Metab.11(8)304-308(2000) 2.Miwa, H., Gantz, I., Konda, Y., et al.Structural determinants of the melanocortin peptides required for activation of melanocortin-3 and melanocortin-4 receptorsJ. Pharmacol. Exp. Ther.273(1)367-372(1995) 3.Cutuli, M., Cristiani, S., Lipton, J.M., et al.Antimicrobial effects of a-MSH peptidesJ. Leukoc. Biol.67(2)233-239(2000) 4.Lipton, J.M., Ceriani, G., Macaluso, A., et al.Antiiinflammatory effect of the neuropeptide a-MSH in acute, chronic, and systemic inflammationAnn. N.Y. Acad. Sci.25(741)137-148(1994)

1-Arachidonoyl lysophosphatidic acid is a phospholipid containing arachidonic acid at the sn-1 position. It has been found in rat brain as 37% of the arachidonic acid-containing lysophosphatidic acid (LPA) species and is a precursor to 1-arachidonoyl glycerol . 1-Arachidonoyl lysophosphatidic acid binds to the LPA2/EDG4 receptor with an EC50 value of approximately 10 nM. It prevents TNF-α and IL-6 secretion in wild-type but not Lpa2-/- dendritic cells stimulated by LPS. It also decreases differentiation of HT-29 human colon carcinoma cells to goblet cells in the presence of sodium butyrate.

Glucocorticoid receptor modulator 1 is a potent, orally active, non-steroidal selective glucocorticoid receptor modulator, exhibiting IC50 values of 9 nM and 130 nM against NF-κB and AP-1, respectively. It effectively reduces the expression of inflammatory factors such as IL-6, IL-1β, and TNF-α, and alleviates dermatitis in mice.

STING agonist-23 (CF502) is a non-nucleotide, small-molecule stimulator of the STING pathway. Upon activation, it enhances the phosphorylation of STING, TBK1, and IRF3, leading to elevated levels of IFN-β, IL-6, CXCL-10, TNF-α, ISG-15, and CCL-5 in tumor cells. Moreover, STING agonist-23 demonstrates efficacy against SARS-CoV series strains [1].

STING agonist-23 (CF505) is a non-nucleotide, small-molecule compound that stimulates STING, enhancing the phosphorylation of STING, TBK1, and IRF3. It elevates the production of IFN-β, IL-6, CXCL-10, TNF-α, ISG-15, and CCL-5 in tumor cells and demonstrates efficacy against SARS-CoV strains [1].

Ansatrienin B is an ansamycin antibiotic and antifungal agent first isolated from S. collinus and S. rishiriensis., In fetal rat long bones, it is an inhibitor of parathyroid hormone-induced calcium release (IC50 = 21 nM), which is a measure of bone resorption, and pp60c-src kinase (IC50 = 50 nM). It is an inhibitor of translation at the protein synthesis stage by specific inhibition of L-leucine incorporation (IC50 = 58 nM in A549 cells). It also inhibits TNF-α-induced expression of intercellular adhesion molecule-1 (ICAM-1; IC50 = 300 nM). Early in vitro studies showed that ansatrienin B potentiates the chemotherapeutic action of 5-fluorouracil , cisplatin , bleomycin , mitomycin C , and 6-mercaptopurine. Ansatrienin B is a hydroquinone form of ansatrienin A .

Anti-Aβ agent 1A is a potent anti-amyloid-β agent. Anti-Aβ agent 1A significantly inhibits LPS-induced IL-1β, IL-6 and TNF-α levels and reduces H2O2-induced apoptosis in SH-SY5Y cells using the mitochondrial pathway, exhibiting antioxidant, anti-inflammatory, anti-Aβ toxicity and neuroprotective activities. Anti-Aβ agent 1A can be used to study Alzheimer's disease.

Euphohelioscopin A, an activator of protein kinase C (PKC), it inhibits proliferation and induces differentiation of the myeloid leukemia cell lines THP-1 and HL-60. Euphohelioscopin A has anti-inflammary activity, it exhibits moderate inhibitory activity

NCI 126224, a toll-like receptor 4 (TLR4) antagonist, demonstrates selective inhibition of nitric oxide (NO) production in RAW 264.7 macrophages, triggered by the TLR4 agonist LPS (IC50 = 0.31 µM), as opposed to minimal effects on NO production induced by agonists for TLR7/8 (R-848), TLR1/2 (Pam3CSK4), and TLR3 (poly(I:C)). Nevertheless, it also effectively inhibits NO production initiated by the TLR2/6 agonist FSL-1 at an IC50 of 0.6 µM in the same cell line. Moreover, NCI 126224 suppresses LPS-induced NF-κB activity in BV-2 microglial cells and reduces LPS-triggered increases in IL-1β and TNF-α levels in RAW 264.7 macrophages with IC50 values of 5.92, 0.42, and 1.54 µM, respectively.

Semapimod is an inhibitor of proinflammatory cytokine production, capable of suppressing TNF-α, IL-1β, and IL-6. It hinders TLR4 signaling with an IC50 of approximately 0.3 μM, impedes p38 MAPK, and reduces nitric oxide production in macrophages. This compound shows promise for treating various inflammatory and autoimmune disorders [1] [2] [3].

PDE4-IN-6 is a safe, potent and moderately selective inhibitor of PDE4, acting on PDE4B (IC50: 0.125 μM) and PDE4D (IC50: 0.43 μM). PDE4-IN-6 is able to down-regulate TNF-α and IL-6 expression levels, exhibits anti-inflammatory and anti-arthritic effects, and has potent immunomodulatory activity. PDE4-IN-6 has potential for anti-rheumatoid arthritis studies.

DCVC inhibits pathogen-stimulated TNF-α in human extra placental membranes in vitro.Target: TNF-αin vitro: DCVC inhibits pathogen stimulated cytokine release from tissue punch cultures. DCVC (5-50 μM) significantly inhibits LTA-, LPS-, and GBS-stimulated cytokine release from tissue cultures as early as 4 h (P ≤ 0.05). In contrast, TCA (up to 500 μM) does not inhibit LTA-stimulated cytokine release from tissue punches. DCVC effects on LTA-stimulated and LPS-stimulated TNF-α release from tissue punch cultures of extraplacental membranes. DCVC effects on GBS-stimulated release of pro-inflammatory cytokines from extraplacental membranes in transwell cultures. [1]. Boldenow E, et al. The trichloroethylene metabolite S-(1,2-dichlorovinyl)-l-cysteine but not trichloroacetate inhibits pathogen-stimulated TNF-α in human extraplacental membranes in vitro. Reprod Toxicol. 2015 Apr;52:1-6. [2]. Lash LH, et al. Multigenerational study of chemically induced cytotoxicity and proliferation in cultures of human proximal tubular cells. Int J Mol Sci. 2014 Nov 18;15(11):21348-65. [3]. Yoo HS, et al. Comparative analysis of the relationship between trichloroethylene metabolism and tissue-specific toxicity among inbred mouse strains: kidney effects. J Toxicol Environ Health A. 2015;78(1):32-49.

Questinol exhibits significant anti-obesity activity. It shows anti-inflammatory effect in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells, it can inhibit the production of pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-6 and inhibit NO an

β5i-IN-1 is a selective inhibitor of β5i, exhibiting potent activity with an IC50 of 8.463 nM. It modulates immune responses by promoting the release of TNF-α and IL-6 and affecting NF-κB transcriptional activity. This compound has applications in the research of idiopathic pulmonary fibrosis [1].

1. Negletein (7-O-Methylbaicalein) has anti-inflammatory and immunomodulatory activities via inhibition of TNF-α, iNOS and IL-1β. 2. Negletein as a neuroprotectant enhances the action of nerve growth factor and induces neurite outgrowth in PC12 cells. 3. Negletein shows a comparable redox-active potential, and it (50 μM, 4 h) can activate Nrf2. 4. Negletein shows significant antimicrobial activity. 5. Negletein has anti-hypoxia activity, it can significantly prolong the survival time of hypoxic mice.6. Negletein has anti- Alzheimer's disease activity, it inhibits the iron-dependent formation of ROS and also blocks the iron-induced oligomerization of amyloid beta 42 in vitro. 7. Negletein (IC50: 3.89 + - 0.39 microM) exhibits potent inhibitory activity against nuclear factor of activated T cells (NFAT) transcription factor.

IQ3 is a selective inhibitor of JNK3(JNK3, JNK1 and JNK2 with Kd of 66 nM, 240 nM and 290 nM, respectively). IQ 3 inhibits NF-κB/AP1 transcriptional activity in THP1-Blue cells with IC50 of 1.4 μM, also inhibits TNF-α and IL-6 production in vitro.

Cathelicidin-2 (CATH-2) (128-153) is a synthetic antimicrobial peptide derived from amino acids 128-153 of chicken CATH-2, demonstrating activity against pathogens such as E. coli, S. aureus, S. enteritidis, and B. globigii in a dose-dependent manner. At a concentration of 40 µM, it induces hemolysis in chicken erythrocytes without exhibiting cytotoxicity towards human peripheral blood mononuclear cells (PBMCs). Additionally, it stimulates the production of the chemokine CCL2 and suppresses LPS-induced secretion of TNF-α, IL-6, IL-8, and IL-10 in human PBMCs.

Rhein-13C4 is intended for use as an internal standard for the quantification of rhein by GC- or LC-MS. Rhein is an anti-inflammatory anthraquinone found in rhubarb and is the bioactive derivative of its prodrug diacerein . At 10 μM, rhein inhibits IL-1β signaling, suppressing signaling through NF-κB, and reduces the expression of the matrix metalloproteases MMP-1 and MMP-13.1 It inhibits IKKβ (IC50 = 11.8 μM), decreasing iNOS and IL-6 expression in LPS-stimulated macrophages but paradoxically increasing TNF-α, IL-1β, and HMBG1 expression.2 Rhein shows efficacy against pancreatic fibrosis, chronic pancreatitis, and hyperglycemia-induced pancreatic β-cell apoptosis.3,4 It also inhibits angiogenesis of breast cancer cells under normoxic and hypoxic conditions.5

COX-2-IN-10 is a potent COX-2 inhibitor that exhibits inhibitory effects on the production of IL-6, TNF-α, and IL-1β, and inhibits PGE2 production in a concentration-dependent manner with an IC50 value of 2.54 μM. Additionally, COX-2-IN-10 inhibits the expression of iNOS and COX-2 at both mRNA and protein levels.

DPP-4-IN-8 (compound 27) is a potent and selective inhibitor of dipeptidyl peptidase 4 (DPP4), with an inhibition constant (Ki) of 0.96 μM. It inhibits the dipeptidase activity of DPP4 in both Caco-2 and HepG-2 cells and dose-dependently reduces the expression of chemokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) [1].

PDE1-IN-5 (Compound 10c) is a selective PDE1C inhibitor with an IC50 of 15 nM, exhibiting anti-inflammatory properties through the inhibition of iNOS, TNF-α, IL-1α, IL-1β, and IL-6 expression induced by LPS. It has demonstrated efficacy in mitigating inflammatory bowel disease (IBD) symptoms in a dextran sodium sulfate (DSS)-induced colitis mouse model, suggesting its potential utility for IBD research [1].

TNF-α-IN-10 (compound 8a) is an inhibitor of IL-6 and TNF-α, exhibiting anti-inflammatory activity [1].

Anti-inflammatory agent 54 (compound 9c), a Coixol derivative, exhibits anti-inflammatory properties by inhibiting the NF-κB pathway and reducing the expression of pro-inflammatory cytokines such as iNOS, TNF-α, IL-6, and IL-1β. It effectively suppresses LPS-induced nitric oxide (NO) production in RAW264.7 macrophages with an IC50 of 2.4 μM and demonstrates in vivo efficacy in a mouse auricular edema model [1].

Compound 9j (anti-inflammatory agent 55), a Coixol derivative, exhibits anti-inflammatory properties by inhibiting the NF-κB pathway and reducing the expression of iNOS, TNF-α, IL-6, and IL-1β. It notably suppresses LPS-induced nitric oxide (NO) production in RAW264.7 macrophages with an IC50 of 0.8 μM and demonstrates anti-inflammatory effects in vivo using a mouse auricular edema model [1].

Gamma-glutamylcysteine (TFA) ((γ-glutamylcysteine (TFA)), a crucial dipeptide in glutathione (GSH) synthesis and a vital cofactor for the enzyme glutathione peroxidase (GPx), significantly modulates inflammatory responses. It enhances the level of the anti-inflammatory cytokine IL-10, diminishes the concentrations of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β), and mitigates alterations in metalloproteinase activity in oligomeric Aβ40-treated astrocytes.

STING agonist-23 (CF508), a non-nucleotide small-molecule STING agonist, activates STING, thereby enhancing the phosphorylation of STING, TBK1, and IRF3. This activation elevates the production of IFN-β, IL-6, CXCL-10, TNF-α, ISG-15, and CCL-5 in tumor cells. Moreover, STING agonist-23 demonstrates efficacy against SARS-CoV series strains [1].

STING agonist-23 (CF510) is a non-nucleotide, small-molecule activator of the STING pathway. It initiates the phosphorylation of STING, TBK1, and IRF3, enhancing the production of IFN-β, IL-6, CXCL-10, TNF-α, ISG-15, and CCL-5 in tumor cells. Notably, it demonstrates activity against SARS-CoV series strains [1].

Taurohyodeoxycholic acid (THDCA) is a taurine-conjugated form of the secondary bile acid hyodeoxycholic acid .1THDCA decreases the size and weight of human gallstonesin vitro. It increases bile flow, biliary cholesterol secretion, and biliary lipid secretion in rats.2Co-administration of THDCA with taurochenodeoxycholic acid prevents TCDCA-induced hepatotoxicity, increasing bile flow as well as biliary acid and phospholipid secretion in rats.3THDCA also reduces myeloperoxidase activity, expression of TNF-α and IL-6, and colonic damage in a mouse model of TNBS-induced ulcerative colitis.4Taurohyodeoxycholic acid MaxSpec standard is a quantitative grade standard of taurohyodeoxycholic acid (sodium salt) that has been prepared specifically for mass spectrometry and related applications where quantitative reproducibility is required. The solution has been prepared gravimetrically and is supplied in a deactivated glass ampule sealed under argon. The concentration was verified by comparison to an independently prepared calibration standard. Verified concentration is provided on the certificate of analysis. This taurohyodeoxycholic acid MaxSpec standard is guaranteed to meet identity, purity, stability, and concentration specifications and is provided with a batch-specific certificate of analysis. Ongoing stability testing is performed to ensure the concentration remains accurate throughout the shelf life of the product.Note: The amount of solution added to the vial is in excess of the listed amount. Therefore, it is necessary to accurately measure volumes for preparation of calibration standards. Follow recommended storage and handling conditions to maintain product quality.

CAY10789 (compound 6) is a potent CysLT1R (cysteinyl leukotriene receptor 1) antagonist with an IC50 of 2.80 μM and a GPBAR1 (G-protein-coupled bile acid receptor 1) agonist with an EC50 of 3 μM. It significantly decreases U937 cell adhesion to HAEC and reduces TNF-α expression. CAY10789 demonstrates promising metabolic stability and excellent pharmacokinetics, making it suitable for studying colitis, metabolic syndromes, and other GPBAR1 CysLT1R-related diseases [1].

NOD2 antagonist 1 (compound 32) is an effective and selective NOD2 antagonist (IC50: 5.23 μM). In THP-1 cells, it represses Muramyl DiDP (MDP)-induced IL-8 secretion and, in PBMCs cells, inhibits MDP-induced elevation of IL-6, IL-10, and TNF-α.

Manumycin A is an antibiotic with anticancer activity and is a mammalian thioredoxin reductase-1 (TrxR-1) inhibitor.Manumycin A inhibits the production of IL-1β, IL-6, and IL-8 in TNF alpha-stimulated THP-1 cells and peripheral blood mononuclear cells in a dose-dependent manner, inducing apoptosis.

Anti-inflammatory agent 64 (compound 4b) demonstrates antioxidant and anti-inflammatory properties, effectively inhibiting IL-6 and TNF-α secretion and reducing paw edema [1] in both in vitro and in vivo studies.

F1, an anti-inflammatory peptide, incorporates the HIV-1 Tat protein transduction domain linked with a 15-amino acid sequence from residues 46-60 of the inhibitor of NF-κB kinase-interacting peptide (IKIP). It effectively blocks LPS-induced phosphorylation of IκB kinase α (IKKα) and IKKβ, along with the nuclear translocation of NF-κB (p65) in mouse peritoneal macrophages at 5 µM concentration. F1, administered at 5 mg/kg in vivo, significantly reduces IL-6, TNF-α, and IL-1β serum levels and enhances survival in a mouse sepsis model induced by LPS.

Pap12-6, an antibacterial peptide originating from the first twelve N-terminal amino acids of papiliocin found in P. xuthus larvae, exhibits activity against a range of eight Gram-negative bacteria (e.g., E. coli, P. aeruginosa, S. syphimurium with MIC50s=4-8 µM) and Gram-positive bacteria (e.g., S. aureus, methicillin-resistant S. aureus 3126, B. subtilis, and S. epidermidis with MIC50s=4-8 µM), without compromising the viability of human erythrocytes, mouse RAW 264.7 macrophages, human HaCaT keratinocytes, or human HEK293 kidney cells at 25 µM. It causes membrane depolarization in E. coli at 4 and 8 µM and, upon preincubation at 10 µM, decreases nitrite (NO2-), Tnf-α, and Il-6 secretion in LPS-stimulated RAW 264.7 macrophages. In a murine model, Pap12-6 enhances survival rates and diminishes colony forming units (CFUs) in several organs upon E. coli infection at 10 mg/kg and 1 mg/kg doses, respectively. Additionally, at a 1 mg/kg dose, it lowers serum aspartate aminotransferase (AST) and alanine transaminase (ALT) levels, as well as blood urea nitrogen levels in E. coli-induced sepsis, indicating its therapeutic potential for bacterial infections without affecting host cell viability.

Metaxalone-d6 is intended for use as an internal standard for the quantification of metaxalone by GC-or LC-MS. Metaxalone is a skeletal muscle relaxant. It inhibits the proliferation of, and induces apoptosis in, RAW 264.7 cells in vitro when used at concentrations ranging from 1 to 100 µM. Metaxalone also reduces LPS-induced increases in COX-1, COX-2, and NF-kB levels and inhibits LPS-induced production of TNF-α, IL-6, and prostaglandin E2 in RAW 264.7 cells. Formulations containing metaxalone have been used in the treatment of lower back pain.

Flufenamic acid-d4 is intended for use as an internal standard for the quantification of flufenamic acid by GC- or LC-MS. Flufenamic acid is a non-steroidal anti-inflammatory drug (NSAID) and COX inhibitor (IC50s = 3 and 9.3 µM for human COX-1 and COX-2, respectively). Flufenamic acid inhibits TNF-α-induced increases in COX-2 levels and NF-κB activation in HT-29 colon cancer cells in a concentration-dependent manner. It inhibits calcium influx induced by fMLP or A23187 in human polymorphonuclear leukocytes (PMN) with IC50 values of 29 and 14 µM, respectively. Flufenamic acid also activates various ion channels, including transient receptor potential canonical 6 (TRPC6) and the large-conductance calcium-activated potassium channel (KCa1.1). It also inhibits various ion channels, including TRPC3 and the cystic fibrosis transmembrane conductance regulator (CFTR). Flufenamic acid (20 mg/kg) reduces increases in intestinal fluid secretion and intestinal barrier disruption in mice ......

JNK2-IN-1 (Compound J27), a selective JNK2 inhibitor with a dissociation constant (Kd) of 79.2 µM, exhibits anti-inflammatory effects by attenuating TNF-α and IL-6 secretion via inhibition of the NF-κB/MAPK pathway. It effectively mitigates symptoms associated with LPS-induced acute lung injury (ALI) and sepsis [1].

Taxamairin B is a potent anti-inflammatory compound that inhibits the expression of proinflammatory cytokines (TNF-α, IL-1β, and IL-6) and reduces the production of NO and ROS in LPS-induced RAW264.7 cells. Additionally, it shows substantial protective effects against LPS-induced acute lung injury in mice [1] [2].