ecm

Pyrintegrin, a β1-integrin agonist, promotes the survival of embryonic stem cells, can be used as a podocyte-protective agent, and enhances cell-extracellular matrix adhesion-mediated integrin signaling.

Avicularin (Fenicularin) has anti-allergic, anti-inflammatory, hepatoprotective, antioxidant, anti-tumor and other activities. It ameliorates human hepatocellular carcinoma by modulating the activities of NF-κB(p65), COX-2, and PPAR-γ. In LPS-stimulated RAW 264.7 macrophages, it exerts anti-inflammatory activity by inhibiting the ERK signaling pathway.

ecMetAP-IN-1 can be used as a QSAR model to study methionine aminopeptidase inhibitor as an anticancer agent using multiple linear regression.

Anti-Mouse E-Cadherin/CD324 Antibody (DECMA-1) is an IgG1, κ inhibitor antibody derived from rats, targeting mouse E-Cadherin/CD324.

BNTA is a potent extracellular matrix (ECM) modulator. In a rat model of arthritis, BNTA modulates arthritis by promoting the synthesis of cartilage structural molecules on chondrocytes through the induction of superoxide dismutase 3 (SOD3) and regulating chondrogenesis through superoxide anion elimination.

ATN-161 acetate, a pentapeptide compound derived from the synergistic region of fibronectin, is a non-competitive integrin-alpha5 antagonist with antitumor activity that attenuates the pathology of caerulein-induced acute pancreatitis.

Fluorofenidone (AKF-PD) attenuates the progression of renal interstitial fibrosis partly by suppressing NADPH oxidase and extracellular matrix (ECM) deposition via the PI3K/Akt signalling pathway. Fluorofenidone is an analogue of AMR69. Which displays equivalent lower toxicity, antifibrotic activity, and longer half-life.

Flunisolide (Rhinalar) is a synthetic corticosteroid with anti-inflammatory and antiallergic properties.

Collagenase Type VIII hydrolyses Type VIII collagen and can be used to study collagen metabolism processes in the pathophysiology of atherosclerosis. Collagenase Type VIII can also hydrolyse other protein components in the extracellular matrix (ECM), making it useful for tissue dissociation and cell separation.

Autotaxin-IN-7 (45) is a pyridine-2-carboxylic acid derivative exhibiting sub-nanomolar inhibition of ATX (IC50 = 0.086 nM) and features excellent cardiac safety (hERG > 30 μM) with minimal toxicity to fibroblasts. It inhibits the TGF-β/Smad signaling pathway, reducing α-smooth muscle actin (α-SMA) and extracellular matrix components (ECM). Autotaxin-IN-7 (45) can be used in pulmonary fibrosis research.

CYD0682 is an analog of Oridonin. It reduces the activation of STAT3 and the production of ECM in hepatic stellate cells via the HSP90 pathway.

Epsilon-(gamma-glutamyl)-lysine is an N(6)-acyl-L-lysine derivative that establishes cross-links between extracellular matrix (ECM) components through the catalytic activity of the enzyme tissue transglutaminase (tTg), and Epsilon-(gamma-glutamyl)-lysine has been implicated in the pathological remodeling of tissues in diseases such as non-diabetic kidney disease and in the progression of glaucoma filtration, rendering it a critical biomarker and mechanistic factor in extracellular matrix biology.

Chrysotobibenzyl, a bibenzyl found in the stem of Dendrobium pulchellum, may facilitate anoikis--a form of programmed cell death that occurs in anchorage-dependent cells when they detach from the surrounding extracellular matrix (ECM)-- and inhibit the growth of lung cancer cells in anchorage-independent condition. Preliminary data obtained discloses the inhibitory effect on cancer cell metastasis of the isolated compounds and may provide a new approach for cancer drug development.

Epsilon-(gamma-glutamyl)-lysine (H-Glu(H-Lys-OH)-OH) TFA, an N(6)-acyl-L-lysine derivative, is crucial in forming epsilon-(gamma-glutamyl)lysine crosslinks within extracellular matrix (ECM) components, facilitated by tissue transglutaminase (tTg), and is significant in diseases like non-diabetic kidney disease and glaucoma filtration [1].

RGD peptide (GRGDNP) TFA functions as an inhibitor of integrin-ligand interactions, competitively blocking α5β1's interaction with the extracellular matrix (ECM). It induces apoptosis by triggering conformational changes that facilitate pro-caspase-3 activation and autoprocessing. Furthermore, RGD peptide (GRGDNP) TFA is critical in regulating cell adhesion, migration, growth, and differentiation [1] [2] [3].

H-Ile-Lys-Val-Ala-Val-OH (IKVAV) is a short peptide with a sequence length of 5, present in the extracellular matrix (ECM), on the α-laminin chain. H-Ile-Lys-Val-Ala-Val-OH participates in a variety of life activities, such as promoting cell adhesion, neurite outgrowth, angiogenesis, collagenase IV production and tumor growth. H-Ile-Lys-Val-Ala-Val-OH can induce rapid differentiation of neural progenitor cells into neurons and neurite outgrowth.

Plasminogen is a zymogen secreted as a precursor protein that, when cleaved by urokinase plasminogen activator (uPA) or tissue plasminogen activator (tPA), is converted into plasmin. Plasmin is a protease with broad specificity, capable of degrading fibrin and various extracellular matrix (ECM) components. Additionally, plasminogen functions as a proinflammatory regulator, promoting the healing of both acute and diabetic wounds. It is utilized in research related to wound healing, inflammation, and hypoplasminogenemia [1] [2].

Myristoyl tetrapeptide Ala-Ala-Pro-Val is a bioactive peptide that promotes the expression of extracellular matrix (ECM) proteins and inhibits metalloproteinases (MMPs).

ALK5-IN-79 (compound 57), an ALK inhibitor, exhibits anticancer activity by inhibiting the TGF-β1/SMAD signaling pathway. It effectively reduces the production of extracellular matrix (ECM) and collagen deposition. Moreover, ALK5-IN-79 demonstrates satisfactory pharmacokinetic (PK) properties and favorable in vivo tolerance.

Endosidine 5 (ES5) inhibits the secretion of EPS (extracellular polymeric substances) and cell wall expansion. It modifies the secretion of ECM (extracellular matrix) materials in Penium margaritaceum by affecting the Golgi apparatus. Additionally, Endosidine 5 disrupts endosomal cycling through Annexin A6, thereby enhancing the release and expression of mRNA into the cytoplasm.

Hyaluronic Acid Methacryloyl (HAMA) with a molecular weight of 150 kDa is a biocompatible methacrylated derivative of hyaluronic acid. HAMA is utilized as an ink for 3D printing hydrogels, exhibiting rapid photoreactive responses, quick gelation speeds, and stable hydrogel properties. Under ultraviolet light exposure, HAMA efficiently induces gelation in conjunction with phenyl-2,4,6-trimethylbenzoylphosphinate (LAP). The integration of HAMA with tissue-specific extracellular matrix (ECM) materials, such as pancreatic ECM (pECM), is poised to become a vital source material for organ-like tissue cultivation.

Hyaluronic acid Methacryloyl (MW 400 kDa) is a methacrylated form of hyaluronic acid that exhibits biocompatibility. It functions as a 3D printing hydrogel ink, characterized by rapid photosensitivity, quick gelation speed, and stable hydrogel properties. Upon UV exposure, it can rapidly initiate gelation with lithium phenyl-2,4,6-trimethylbenzoylphosphinate (LAP). Additionally, when combined with tissue-specific extracellular matrix (ECM) materials, such as pancreatic extracellular matrix (pECM), Hyaluronic acid Methacryloyl (MW 400 kDa) serves as a crucial source material for organoid culture.

Hyaluronic acid methacryloyl (MW 300000) (HAMA (MW 300000)) is a natural extracellular matrix (ECM) with anti-inflammatory properties that promotes cell adhesion and proliferation. This compound is extensively used in tissue engineering and regenerative medicine. Upon exposure to ultraviolet light, Hyaluronic acid methacryloyl (MW 300000) (HAMA (MW 300000)) quickly forms a hydrogel.

Dencichine (ODAP) is a neurotoxic agent. Dencichine is a haemostatic agent, the hemostatic effect relates to modulation of the coagulation system, platelet aggregation and fibrinolytic system. It has renoprotective effect, it could significantly prevent the progression of diabetic nephropathy possibly attribute to down-regulation of the TGF-β/Smad pathway and rebalance the deposition and degradation of ECM proteins.