2. Immunology/Inflammation NF-κB Apoptosis Cell Cycle/DNA Damage
  3. Toll-like Receptor (TLR) NF-κB TNF Receptor MyD88 Apoptosis DNA/RNA Synthesis
  4. CRX 527

CRX 527 is a TLR4 agonist. CRX 527 activates the MyD88-dependent, TRIF-dependent, and TRAF6/NF-κB signaling pathways downstream of TLR4, mimics lipid A, and regulates antigen processing and presentation by dendritic cells. CRX 527 stimulates innate immune responses and enhances vaccine efficacy. CRX 527 maintains the structural integrity of hematopoietic tissues, spleen and intestine, alleviates radiation-induced damage, preserves intestinal homeostasis, and inhibits apoptosis, inflammatory responses, oxidative stress and DNA damage. CRX 527 can be used in the research of acute radiation syndrome, melanoma, HPV-related tumors and intracerebral hemorrhage.

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CRX 527

CRX 527 Chemical Structure

CAS No. : 216014-14-1

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CRX 527 Related Antibodies

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RNASE L DNA Polymerases RNA Polymerases Helicases DNA Ligase

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Description

CRX 527 is a TLR4 agonist. CRX 527 activates the MyD88-dependent, TRIF-dependent, and TRAF6/NF-κB signaling pathways downstream of TLR4, mimics lipid A, and regulates antigen processing and presentation by dendritic cells. CRX 527 stimulates innate immune responses and enhances vaccine efficacy. CRX 527 maintains the structural integrity of hematopoietic tissues, spleen and intestine, alleviates radiation-induced damage, preserves intestinal homeostasis, and inhibits apoptosis, inflammatory responses, oxidative stress and DNA damage. CRX 527 can be used in the research of acute radiation syndrome, melanoma, HPV-related tumors and intracerebral hemorrhage[1][2][3][4].

In Vitro

CRX 527 (1-100 ng/mL; 24 h) upregulates IL-2R expression on bovine peripheral blood γδ T cells in vitro, with the strongest response observed at 100 ng/mL[1].
CRX 527 (12 h) activates murine RAW264.7 and human THP-1 macrophages, and protects murine MODE-K and human HIEC intestinal epithelial cells against ionizing radiation-induced damage by reducing apoptosis, inflammatory responses and ROS production[2].
CRX 527 (2-12 h) activates the TLR4-MyD88 and TLR4-TRIF signaling pathways in murine RAW264.7 macrophages[2].
CRX 527 (0.04-500 nM; 24 h) retains TLR4 activation activity after conjugation with OVA CTL or OVA helper peptides, and induces IL-12p40 production in D1 dendritic cells, with potency comparable to that of free CRX-527[3].
Conjugation of CRX 527 (427-3500 nM; overnight) with OVA CTL peptide enhances MHC class I antigen presentation of the SIINFEKL epitope by D1 dendritic cells, and the intensity of B3Z reporter T cell activation induced by this conjugate is higher than that induced by free peptide or CRX-527-peptide mixture[3].
When conjugated with OVA helper peptides, CRX 527 (78.1-5000 nM; overnight) enhances the MHC class II antigen presentation of OVA helper T cell epitopes by D1 dendritic cells, and the intensity of OTIIZ reporter gene T cell activation it induces is higher than that induced by free peptides or CRX-527-peptide mixtures[3].
When conjugated to the OVA CTL peptide, CRX 527 (7.8-500 nM; 50 h) enhances the activation of naive OT-I CD8+ T cells co-cultured with peptide-pulsed D1 dendritic cells, as well as the production of multifunctional cytokines (IFNγ and TNFα), and exhibits greater potency than free peptide or the CRX-527-peptide mixture[3].
When conjugated with OVA helper peptide, CRX 527 (31-2000 nM; 50 h) enhances the activation of naive OT-II CD4+ T cells co-cultured with peptide-pulsed D1 dendritic cells, as well as the production of multifunctional cytokines (IFNγ and TNFα), and exhibits greater potency than free peptide or CRX-527-peptide mixture[3].
When conjugated with the EnvH peptide, CRX 527 (78.1-5000 nM; 50 h) enhances MHC class II antigen presentation of the EnvH epitope by D1 dendritic cells. Compared with free peptide or CRX-527-peptide mixture, it induces stronger activation of 3A12 reporter T cells and promotes TNFα production by naive MolH CD4+ T cells[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

CRX 527 Related Antibodies

ELISA Assay[3]

Cell Line: mouse spleen-derived immature D1 DC cell line
Concentration: 0.04, 0.2, 1, 5, 20, 500 nM
Incubation Time: 24 h
Result: Induced IL-12p40 production in D1 DCs in a concentration-dependent manner, with levels comparable to free CRX-527.
Induced ~7 ng/mL IL-12p40 at 500 nM when conjugated to OVA CTL peptide.
Induced ~7 ng/mL IL-12p40 at 500 nM when conjugated to OVA Help peptide.
Induced ~8 ng/mL IL-12p40 at 500 nM in free form.
In Vivo

CRX 527 (1 μg; i.t.; single dose) induces a more robust lung neutrophil recruitment than lipo-CRX, LPS, or MPL in healthy C57BL/6 mice, with no effect on blood neutrophil or macrophage percentages[1].
CRX-527 (0.5 mg/kg; i.p.; twice) confers 100% survival in C57BL/6 mice subjected to 7.5 Gy total body irradiation, while effectively alleviating ionizing radiation-induced hematopoietic system damage[2].
CRX-527 (0.5 mg/kg; i.p.; twice) activates hematopoietic mobilization and immune-favorable differentiation of hematopoietic stem cells in C57BL/6 mice, increasing LSK and GMP populations while reducing immunosuppressive MDSCs[2].
CRX-527 (0.5 mg/kg; i.p.; twice) increases bone marrow macrophage proportions and preserves peripheral blood white blood cell counts in C57BL/6 mice subjected to 5Gy total body irradiation, activating macrophage-mediated immune defense[2].
CRX-527 (0.5 mg/kg; i.p.; twice) confers 80% survival in C57BL/6 mice subjected to 9 Gy local abdominal irradiation, while protecting intestinal homeostasis, stem cell regeneration, and barrier function from ionizing radiation damage[2].
CRX-527 (0.5 mg/kg; i.p.; twice) does not protect against ionizing radiation-induced hematopoietic or intestinal injury in TLR4 knockout mice, indicating its radioprotective effects are mediated via TLR4 activation[2].
Prophylactic vaccination with CRX 527 (2 nmol; i.d.; twice (day 0, day 14))-peptide conjugates, particularly the combined CTL + T-helper conjugate, induces robust tumor-specific CD8 T cell responses and confers ~90% long-term survival in mice challenged with B16OVA melanoma[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6 (6- to 10-week-old, mixed male and female, approximately equal numbers, 5 mice per group)[1]
Dosage: 1 μg
Administration: i.t.; single dose
Result: Induced a more robust lung neutrophil influx than lipo-CRX, LPS, or MPL.
Did not alter blood neutrophil or macrophage percentages at 24 hours post-treatment.
Animal Model: C57BL/6 (weight 18-20 g; total body irradiation with 7.5 Gy X-ray)[2]
Dosage: 0.5 mg/kg
Administration: i.p.; twice (24 hours and 2 hours pre-irradiation)
Result: Increased post-irradiation survival rate to 100% (compared to 50% in untreated irradiated mice).
Showed more gradual weight changes, preserved higher bone marrow nucleated cell counts, higher spleen coefficients, greater numbers of LSK (lin-sca-1+ c-kit+) cells, more intact bone marrow hematopoietic microenvironment with fewer vacuoles, more complete blood sinus structure, and higher spleen white pulp cell density relative to untreated irradiated mice.
Animal Model: C57BL/6[2]
Dosage: 0.5 mg/kg
Administration: i.p.; twice (24 hours and 2 hours prior to sample collection)
Result: Increased the proportion and number of LSK (Lin-sca-1+ c-kit+) cells.
Reduced the proportion of long-term hematopoietic stem cells (LT-HSCs, CD34- CD135- LSK) and increased the proportion of short-term hematopoietic stem cells (ST-HSCs, CD34+ CD135- LSK) and multipotent hematopoietic progenitors (MPPs, CD34+ CD135+ LSK).
Promoted differentiation of hematopoietic progenitor cells (HPCs) into granulocyte/monocyte progenitor cells (GMPs, FcRhighCD34+ LK).
Decreased the proportion of bone marrow-derived inhibitory cells (MDSCs, CD45+ Gr-1+ CD11b+).
Animal Model: C57BL/6 (total body irradiation with 5 Gy X-ray)[2]
Dosage: 0.5 mg/kg
Administration: i.p.; twice (24 hours and 2 hours pre-irradiation)
Result: Maintained higher peripheral blood white blood cell counts throughout the observation period post-irradiation.
Increased the proportion of bone marrow macrophages (CD11b+ F4/80+) relative to untreated irradiated mice.
Animal Model: C57BL/6 (local abdominal irradiation with 9 Gy X-ray)[2]
Dosage: 0.5 mg/kg
Administration: i.p.; twice (24 hours and 2 hours pre-irradiation)
Result: Increased post-irradiation survival rate to 80% (compared to 0% in untreated irradiated mice).
Showed more gradual weight changes, preserved intestinal crypt-villus structure, maintained higher counts of Lgr5+ intestinal stem cells, Lysozyme+ Paneth cells, and Ki67+ epithelial regeneration cells, more complete villin expression, higher fecal quantity and weight without watery/loose stools, retained higher ZO-1 expression to preserve intestinal barrier function, suppressed 8-OHdG oxidative stress marker levels, and reduced intestinal tissue expression of PARP, IL-1β, IL-6, TNF-α, and Caspase-3 relative to untreated irradiated mice.
Animal Model: TLR4 knockout (TLR4-/-) (total body irradiation with 7.5 Gy and 5 Gy X-ray)[2]
Dosage: 0.5 mg/kg
Administration: i.p.; twice (24 hours and 2 hours pre-irradiation)
Result: Had no significant effect on post-irradiation survival rate, body weight changes, spleen coefficient, bone marrow nucleated cell counts, spleen nucleated cell counts, peripheral blood white blood cell counts, LSK cell proportions, GMP cell proportions, MDSC cell proportions, bone marrow macrophage proportions, intestinal F4/80 macrophage levels, or intestinal crypt counts in irradiated TLR4-/- mice relative to untreated irradiated TLR4-/- mice.
Animal Model: Sprague-Dawley (SD) (220-250 g)[4]
Dosage: 0.25 mg/kg
Administration: i.p.; single dose (before ICH injury)
Result: Reversed the NR4A2-mediated reduction in BBB permeability by increasing FITC-dextran penetration, perivascular IgG accumulation, and Evans blue extravasation in ICH rats.
Reversed the NR4A2-mediated suppression of ICH-induced increases in P-selectin, ICAM-1, CXCL1, and CCL2 mRNA levels in perihematomal tissues.
Counteracted the NR4A2-driven shift toward M2 microglial polarization by increasing levels of M1 markers (iNOS, CD86) and decreasing levels of M2 markers (CD206, Arg-1) in perihematomal tissues.
Reversed the NR4A2-mediated suppression of the TLR4/TRAF6/NF-κB pathway, increasing protein levels of TLR4, TRAF6, and p-NF-κB p65.
Exacerbated ICH-induced BBB disruption, increased inflammatory marker expression, promoted M1 microglial polarization, and enhanced activation of the TLR4/TRAF6/NF-κB pathway when administered alone.
Molecular Weight

1488.04

Formula

C81H151N2O19P
CAS No.
SMILES

CCCCCCCCCC(O[C@H](CCCCCCCCCCC)CC(O[C@@H]1[C@H]([C@@H](O[C@@H]([C@H]1OP(O)(O)=O)CO)OC[C@@H](C(O)=O)NC(C[C@@H](CCCCCCCCCCC)OC(CCCCCCCCC)=O)=O)NC(C[C@@H](CCCCCCCCCCC)OC(CCCCCCCCC)=O)=O)=O)=O
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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

CRX 527216014-14-1CRX527CRX-527Toll-like Receptor (TLR)NF-κBTNF ReceptorMyD88ApoptosisDNA/RNA SynthesisNuclear factor-κBNuclear factor-kappaBTumor Necrosis Factor ReceptorTNFRTLR4C57BL/6 miceTRIFBrucella abortusTRAF6/NF-κBhematopoietic stem cellsTHP-1 macrophagesdendritic cellsRAW264.7 macrophagesInhibitorinhibitorinhibit

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