1. Signaling Pathways
  2. Cytoskeleton
  3. Collagen
  4. Collagen I Isoform

Collagen I

 

Collagen I Related Products (12):

Cat. No. Product Name Effect Purity
  • HY-P990294
    Anti-Mouse CD106/VCAM-1 Antibody (M/K-2.7)
    Inhibitor
    Anti-Mouse CD106/VCAM-1 Antibody (M/K-2.7) is an anti-mouse CD106/VCAM-1 IgG1 monoclonal antibody. Anti-Mouse CD106/VCAM-1 Antibody (M/K-2.7) reduces inflammatory response and oxidative stress by lowering p-STAT3 and reactive oxygen species (ROS) levels. Anti-Mouse CD106/VCAM-1 Antibody (M/K-2.7) can alleviate cardiac inflammation and fibrosis by reducing the expression of collagen I and collagen III. Anti-Mouse CD106/VCAM-1 Antibody (M/K-2.7) can be used for research on cardiovascular conditions such as hypertensive heart condition and subretinal fibrosis.
  • HY-163121
    PST3.1a
    PST3.1a is an orally active and brain-penetrant N-acetylglucosamine glycosyltransferase (MGAT5) inhibitor with a human IC50 of 2 µM. PST3.1a inhibits TGFβR and FAK signaling pathway activity. PST3.1a alters β1,6-GlcNAc N-glycans and microtubule/microfilament integrity, increases OLIG2 expression, and inhibits proliferation, migration, invasiveness, and clonogenic capacities of glioblastoma initiating cells. PST3.1a reduces invasive and proliferative capacity of glioblastoma initiating cells in orthotopic graft models, increases overall survival of orthotopic graft model mice. PST3.1a blunts MGAT5 overexpression, decreases renal fibrosis via collagen 1, collagen 4, and galectin 3 downregulation in a rat chronic kidney disease model. PST3.1a can be used for the research of glioblastoma multiforme and chronic kidney disease.
  • HY-P5237
    Tetrapeptide-4
    Activator 99.54%
    Tetrapeptide-4 is a synthetic tetrapeptide. Tetrapeptide-4 upregulates hyaluronic acid synthetase, and collagen production in human dermal fibroblasts. Tetrapeptide-4 reduces skin aging, improves skin firmness, elasticity, and appearance, and benefits hair.
  • HY-N17650
    Salviamarinic acid A
    Inhibitor
    Salviamarinic acid A is a water-soluble phenolic acid that can be extracted from Salvia miltiorrhiza with potent anti-pulmonary fibrosis activity. Salviamarinic acid A significantly increases cell viability, cell index, cell motility and E-cadherin expression, and reduces TGF-β1, α-SMA and Collagen I levels. Salviamarinic acid A can be used for pulmonary fibrosis research.
  • HY-P11826
    T2 peptide-1
    Inhibitor
    T2 peptide-1 is a linear peptide derived from Lumican degradation. T2 peptide-1 exhibits activity against endometrial adhesion progression and ability to inhibit the LumicanCollagen I interaction. T2 peptide-1 can be used for the research of liver fibrosis.
  • HY-181993
    JNK3-IN-11
    JNK3-IN-11 is a selective JNK3 inhibitor with an IC50 of 2.08 nM. JNK3-IN-11 binds to the JNK3 ATP-binding pocket, forming conserved hydrogen bonds with Met149 and a water-mediated hydrogen bond with Lys93. JNK3-IN-11 suppresses TGF-β1-induced c-Jun phosphorylation, reduces profibrotic markers COL1A1 and PAI-1, restores E-cadherin expression, and has protection against podocyte injure. JNK3-IN-11 can be used for the research of chronic kidney disease.
  • HY-182904
    GV-001
    Inhibitor
    GV-001 is a selective and orally active HDAC6 inhibitor with an IC50 of 1.18 nM against HDAC6. GV-001 selectively enhances α-tubulin acetylation, reduces sIL-6 and Collagen I levels, suppresses renal cyst growth, and upregulates PC1 expression. GV-001 can be used for the study of autosomal dominant polycystic kidney disease (ADPKD).
  • HY-123958
    SB772077B
    Inhibitor
    SB772077B is a ROCK inhibitor. SB772077B has an anti-inflammatory activity and enhances aqueous outflow facility (OF) by inactivating RhoA/ROCK signal pathway. SB772077B significantly reduces the mRNA level of β-catenin and protein level of fibrotic markers, such as vinculin, fibronectin, collagen 1 A and vimentin. SB772077B also has vasodialatory activity and decreases pulmonary and systemic blood pressure. SB772077B can be used for glaucoma research and pulmonary hypertensive disorder research.
  • HY-180336
    LM9
    Inhibitor
    LM9 is a potent, orally active MyD88 inhibitor. LM9 blocks TLR4/MyD88 binding, MyD88 homodimer formation, and TLR4/MyD88/NF-κB signaling pathway activation. LM9 prevents atherosclerosis by regulating inflammatory responses and oxidative stress in macrophages. LM9 efficiently mitigates inflammatory responses and fibrosis in obesity-induced cardiomyopathy. LM9 can be used for fibrosis and atherosclerosis research.
  • HY-176194
    Antifibrotic agent 1
    Chemical
    Antifibrotic agent 1 is an orally active anti-idiopathic pulmonary fibrosis (IPF) agent. Antifibrotic agent 1 effectively attenuates IPF-related processes, including TGF-β induced EMT and FMT processes, as well as pro-fibrotic M2 polarization. Antifibrotic agent 1 selectively inhibits CSF-1R, PDGFR-α and Src family kinases (SFKs), while sparing VEGFRs, FGFRs and Abl to minimize off-target toxicity. Antifibrotic agent 1 has potent anti-fibrotic activity in Bleomycin (BLM) (HY-108345)-induced pulmonary fibrosis mice model.
  • HY-N11736
    12-O-Tiglyl-phorbol 13-dodecanoate
    Inhibitor
    12-O-Tiglyl-phorbol 13-dodecanoate (TD13) is a potential inhibitor with anti-hepatic fibrosis activity, and it belongs to a series of derivatives of oral APOL2 inhibitors and anti-hepatic fibrosis agents. It shows no obvious toxicity in preclinical models. Compounds of the 12-O-Tiglyl-phorbol 13-dodecanoate series inhibit the expression of fibronectin, type I collagen and α-smooth muscle actin in hepatic stellate cells. 12-O-Tiglyl-phorbol 13-dodecanoate can be isolated from the Euphorbiaceae plant Euphorbia fischeriana, and it is applicable to the research of hepatic fibrosis.
  • HY-167201
    2ccPA
    Inhibitor
    2ccPA is a Cyclic phosphatidic acid derivative. 2ccPA decreases ECM expression, increases the intracellular cAMP levels. 2ccPA decreases the protein expression levels of type I collagen, CCN2 and αSMA. 2ccPA has inhibitory effects on the progression of skin fibrosis by abrogating ECM production from activated skin fibroblasts.