2. Disease Areas
  3. Inflammation or Immune System Disease
  4. Autoimmune Disease
  5. Crohn's Disease

Crohn's Disease

Crohn's disease is a chronic, relapsing inflammatory bowel disease characterized by transmural granulomatous inflammation that can affect any part of the gastrointestinal tract from the mouth to the anus, with a predilection for the terminal ileum, colon, and perianal region. It results from an abnormal immune response leading to persistent inflammation, causing symptoms such as abdominal pain, diarrhea, weight loss, fatigue, and blood in stool. Complications include intestinal strictures, fistulas, abscesses, malnutrition, and an increased risk of colorectal cancer. Although the exact cause remains unknown, genetic, environmental, and immunological factors contribute to its development, with higher incidence among individuals under 30 and those of Jewish descent. While there is no cure, treatment strategies—including medications (aminosalicylates, corticosteroids, immunomodulators, biologics), surgery, and lifestyle modifications—help manage symptoms and prevent complications, enabling most patients to maintain a good quality of life.

Crohn's Disease (14):

Cat. No. 상품명 CAS No. Purity 화학구조
  • HY-156454
    UCB-6876 637324-45-9 98.49%
    UCB-6876 is a TNFα inhibitor. UCB-6876 specifically binds to the asymmetric crystalline form of TNF-α trimer with a KD of 22 μM. UCB-6876 is applicable to research related to autoimmune diseases (rheumatoid arthritis and Crohn's disease).
    UCB-6876
  • HY-108610A
    Edelfosine 70641-51-9 99.0%
    Edelfosine (ET-18-OCH3) is an orally active lipid raft modulator and apoptosis inducer that alters membrane fluidity and preferentially inserts into tumor cell membranes. Edelfosine recruits death receptor ligands (FasL/CD95L, TRAIL) and Bid to lipid rafts to form death-inducing signaling complexes, thereby initiating mitochondria-dependent apoptosis and inducing cytochrome c release. Edelfosine also exerts anti-inflammatory effects, promotes L-Selectin shedding, and causes no gastrointestinal or organ toxicity. In addition, Edelfosine inhibits nucleic acid and protein synthesis in Leishmania donovani and exhibits antiproliferative activity. Edelfosine can be used in research on multiple myeloma, inflammatory bowel diseases (such as ulcerative colitis and Crohn's disease), and visceral leishmaniasis.
    Edelfosine
  • HY-P5522A
    TriDAP dihydrochloride 99.16%
    TriDAP dihydrochloride (L-Ala-γ-D-Glu-meso-diaminopimelic acid dihydrochloride) is a NOD1 agonist with a Kd value of 34.5 μM. TriDAP dihydrochloride enhances the binding of NOD1-RICK, promotes RICK phosphorylation, and activates the NF-κB, TAK1, MEK/ERK, p38 and interferon response pathways. TriDAP dihydrochloride downregulates Runx2 via increasing ubiquitination and reduces trabecular bone parameters. TriDAP dihydrochloride decreases IκBα levels and increases p65 levels. TriDAP dihydrochloride induces the secretion of proinflammatory mediators IL-8 and prostaglandins, triggers tissue inflammation and innate immune activation, and inhibits SARS-CoV-2 replication in lung epithelial cells. TriDAP dihydrochloride increases the RANKL/OPG ratio in mice, reduces bone mass and enhances osteoclast activity, and inhibits new bone formation by decreasing the mineralization deposition rate in mice. TriDAP dihydrochloride can be used in research related to pulpitis, chronic ulcerative colitis, Crohn's disease and SARS-CoV-2 infection.
    TriDAP dihydrochloride
  • HY-P5522
    TriDAP 877462-71-0
    TriDAP (L-Ala-γ-D-Glu-meso-diaminopimelic acid) is a NOD1 agonist with a Kd value of 34.5 μM. TriDAP enhances the binding of NOD1-RICK, promotes RICK phosphorylation, and activates the NF-κB, TAK1, MEK/ERK, p38 and interferon response pathways. TriDAP downregulates Runx2 via increasing ubiquitination and reduces trabecular bone parameters. TriDAP decreases IκBα levels and increases p65 levels. TriDAP induces the secretion of proinflammatory mediators IL-8 and prostaglandins, triggers tissue inflammation and innate immune activation, and inhibits SARS-CoV-2 replication in lung epithelial cells. TriDAP increases the RANKL/OPG ratio in mice, reduces bone mass and enhances osteoclast activity, and inhibits new bone formation by decreasing the mineralization deposition rate in mice. TriDAP can be used in research related to pulpitis, chronic ulcerative colitis, Crohn's disease and SARS-CoV-2 infection.
    TriDAP
  • HY-168990
    Ontunisertib 2647949-48-0 99.95%
    Ontunisertib (AGMB-129) is an orally active and selective gastrointestinal-restricted ALK5 (TGFβR1) inhibitor. Ontunisertib blocks signalling of the pro-fibrotic TGFβ pathway. Ontunisertib can be used for the research of fibrostenotic Crohn’s disease.
    Ontunisertib
  • HY-P99404
    Quetmolimab 2084037-83-0 99.9%
    Quetmolimab (E6011) is a humanized anti-Fractalkine (CX3CL1) monoclonal antibody. Quetmolimab binds to membrane-bound and soluble Fractalkine, neutralizes Fractalkine-induced migration of CX3CR1-expressing cells, mediates target-bound complex elimination from serum. Quetmolimab suppresses free soluble Fractalkine levels in cynomolgus monkeys, with target engagement linked to increased serum total Fractalkine concentration. Quetmolimab can be used for the research of Crohn’s disease, rheumatoid arthritis, and primary biliary cholangitis.
    Quetmolimab
  • HY-123925
    CSLP43 2244988-80-3
    CSLP43 is a selective RIPK2 and XIAP inhibitor with an IC50 of 19.9 nM against human RIPK2. CSLP43 binds to the ATP-binding pocket of RIPK2 and disrupts the interaction between RIPK2 and the BIR2 domain of XIAP or cIAP1. CSLP43 inhibits RIPK2 ubiquitination, NOD1-dependent inflammatory signaling pathways, NOD2-dependent inflammatory signaling pathways, as well as NF-κB activation associated with NOD agonists. CSLP43 is selective for the NOD1/NOD2 signaling pathway and does not inhibit the kinase activity of RIPK1 or RIPK3. CSLP43 is applicable to research related to Crohn's disease, Blau syndrome, early-onset sarcoidosis and early-onset inflammatory bowel disease.
    CSLP43
  • HY-181287
    PROTAC CCR9 Degrader 1
    PROTAC CCR9 Degrader 1 is a PROTAC-based degrader targeting CCR9. PROTAC CCR9 Degrader 1 induces ubiquitination, proteasomal degradation of CCR9 and reduces intracellular CCR9 levels by recruiting the VHL E3 ligase. PROTAC CCR9 Degrader 1 has a Ki value of 78.0 nM against human CCR9. PROTAC CCR9 Degrader 1 modulates GPCR activity by binding to the intracellular allosteric binding site of CCR9. PROTAC CCR9 Degrader 1 can be used in research related to Crohn's disease.
    PROTAC CCR9 Degrader 1
  • HY-105671
    Balazipone 137109-71-8
    Balazipone is a phenylmethylene-2,4-pentanedione compound with anti-inflammation activity. Balazipone can be used for digestive system diseases research, such as Crohn's disease.
    Balazipone
  • HY-N2896
    Arjunolic acid 465-00-9 98.83%
    Arjunolic acid is an orally active, multifunctional bioactive compound. Arjunolic acid exhibits free radical scavenging activity, as well as fungal and bacterial activities. Arjunolic acid induces apoptosis (Apoptosis) in various cancer cells. Arjunolic acid protects hepatocytes against induced oxidative stress and apoptosis by reducing reactive oxygen species and inhibiting NF-κB activation. Arjunolic acid regulates pancreatic dysfunction in type 2 diabetic rats by blocking the activation of the TLR-4/MyD88 and canonical Wnt pathways. Arjunolic acid inhibits neuroinflammation and ameliorates depressive behaviors via the SIRT1/AMPK/Notch1 signaling pathway in microglia. Arjunolic acid improves Crohn's disease-like colitis by restoring gut microbiota composition and inhibiting TLR4 signaling. Arjunolic acid suppresses osteosarcoma progression by inhibiting Wnt3a-mediated M2 polarization of macrophages. Arjunolic acid ameliorates diabetic retinopathy via the autophagy pathway regulated by AMPK/mTOR/HO-1. Arjunolic acid is applicable to research related to type 2 diabetes, organ toxicity, depression, Crohn's disease, osteosarcoma, diabetic retinopathy, and testicular dysfunction.
    Arjunolic acid
  • HY-P11017
    LNSMGQD 1152066-26-6 99.92%
    LNSMGQD is a cyclic peptide fragment derived from desmoglein 1 (amino acids 81-86), which mimics trans-interactions and acts as part of the tandem peptide binding interface of desmoglein 2. LNSMGQD not only binds to desmoglein 1 and 3, but also effectively inhibits their homophilic trans-interactions, while reducing the probability of homophilic or heterophilic binding between desmoglein 2 and Dsc2, N-cadherin and E-cadherin. LNSMGQD is applicable to the research on disease mechanisms such as Crohn's disease and pemphigus vulgaris.
    LNSMGQD
  • HY-N2199
    Sotetsuflavone 2608-21-1
    Sotetsuflavone is a flavonoid that can be isolated from Cycas revolute. Sotetsuflavone inhibits phosphorylation of PI3K, Akt, mTOR, JNK, and p38 MAPK; modulates expression of Cyclin D1, CDK4, Bcl-2, Bax, cleaved caspases 3/9, MMP-9, TGF-β, STAT3, and β-catenin. Sotetsuflavone induces G0/G1 cell cycle arrest, apoptosis, autophagy, and intracellular ROS elevation, inhibits cancer cell proliferation. Sotetsuflavone inhibits tumor growth in mouse tumor xenograft models. Sotetsuflavone can be used for the research of non-small cell lung cancer and Crohn’s disease.
    Sotetsuflavone
  • HY-122142
    Pyr-​Pro-​Arg-​pNA 72194-57-1
    Pyr-​Pro-​Arg-​pNA (S-2366) is a chromogenic peptidyl substrate, and a noncompetitive inhibitor that occupies the active sites of FXIa and FXIa-LC to block factor IX activation. Pyr-​Pro-​Arg-​pNA functions as a hydrolyzable substrate for FXIa’s catalytic domain, human APC, murine APC, and purified plasma kallikrein.
    Pyr-​Pro-​Arg-​pNA
  • HY-185172
    PDE4-IN precursor 2750575-21-2
    PDE4-IN precursor (Compound 10) is an orally active prodrug of phosphodiesterase 4 (PDE4) inhibitor. PDE4-IN precursor undergoes enzymatic hydrolysis in the colon to release the active PDE4 inhibitor, which exerts local anti-inflammatory effects on the colonic mucosa. PDE4-IN precursor is applicable to research related to ulcerative colitis, Crohn's disease, and other relevant conditions.
    PDE4-IN precursor