PDIC-DPC
PDIC-DPC is a HMGA1 inhibitor and lung-targeting agent. PDIC-DPC upregulates STING expression and enhances STING-mediated immune signaling. PDIC-DPC inhibits the TGFβ-Smad pathway and activates AMPK. PDIC-DPC forms nanocomplexes with fibrinogen β chain and vitronectin, and achieves lung-specific accumulation by binding to pulmonary endothelial receptors. PDIC-DPC reverses established pulmonary fibrosis, reduces collagen deposition, restores alveolar structure, improves pulmonary function, and inhibits in situ ESCC growth. PDIC-DPC can be used for the research of esophageal squamous cell carcinoma and idiopathic pulmonary fibrosis.
Para uso exclusivo en investigación. No vendemos a pacientes.
- No. CAS: 3008320-14-4
- Fòrmula: C34H30Cl6N4O4
- Peso molecular:771.34
-
Almacenamiento:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
-
Actividad biológica
-
Chemical Information
- Pureza y Documentación
- Referencias
-
Help & FAQs
Ver todos los productos específicos de isoformas AMPK
More
Actividad biológica
|
HMGA1 |
PDIC-DPC potently inhibits murine AKR ESCC cell viability with an IC50 of 0.542 µmol/L[1].
PDIC-DPC potently inhibits human KYSE-30 ESCC cell viability with an IC50 of 0.709 µmol/L[1].
PDIC-DPC (0.25-1.25 μmol/L) dose-dependently reduces HMGA1 expression and increases STING expression in murine AKR ESCC cells[1].
PDIC-DPC (0.625-10.0 μM) binds strongly to purified vitronectin protein with a Kd of 1.93 μM[2].
PDIC-DPC binds to purified fibrinogen beta chain protein with a dissociation constant of 24.7 μM, showing weaker affinity than for vitronectin[2].
PDIC-DPC binds to multiple mouse plasma proteins, with the highest enrichment for fibrinogen beta chain (9.70%) and vitronectin (2.49%), showing 3.5-fold and 13.8-fold higher abundance than in PBS-treated plasma, respectively[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
PDIC-DPC (2 mg/kg; i.v.; every 3 days) significantly reduces lung metastasis of HMGA1-overexpressing ESCC, enhances CD3+, CD8+, and GzmB+ T cell infiltration in metastatic foci, and prolongs survival in C57BL/6 mice[1].
PDIC-DPC (2 mg/kg; i.v.; every 10 days; 4 months) reduces orthotopic ESCC burden, suppresses HMGA1 expression, and enhances T lymphocyte infiltration in 4NQO-induced ESCC models in both wild-type and HMGA1 knock-in mice[1].
PDIC-DPC (every two days; 14 days) achieves superior reversal of bleomycin-induced pulmonary fibrosis in C57BL/6N mice, as evidenced by a 1.4 Ashcroft score, 96% pulmonary function recovery relative to normal mice, and 100% survival rate, via activation of AMPK and suppression of the TGFβ-Smad pathway[2].
PDIC-DPC (20 mg/kg; daily; 28 days) exhibits highly selective lung accumulation in healthy C57BL/6N mice, with excellent in vivo biocompatibility at doses up to 20 mg/kg over 28 days[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:C57BL/6 background Hmga1KI/KI (wild-type control, 6-8 weeks old, 3 males and 3 females per group, 80 mg/L 4NQO in drinking water for 5 months to induce orthotopic ESCC); C57BL/6 background Hmga1KI/KIK14 (HMGA1 conditional knock-in, 6-8 weeks old, 3 males and 3 females per group, 80 mg/L 4NQO in drinking water for 5 months to induce orthotopic ESCC)[1]
-
Dosage:2 mg/kg
-
Administration:i.v.; every 10 days; 4 months
-
Result:Reduced tumor burden and normalized esophageal pathology in both wild-type and HMGA1 knock-in mice.
Significantly suppressed HMGA1 expression in esophageal tissues.
Increased infiltration of CD3+, CD8+, and GzmB+ T cells in esophageal tissues.
-
Animal Model:C57BL/6N mice[2]
-
Dosage:20 mg/kg
-
Administration:daily; 28 days
-
Result:Showed dominant accumulation in the lung, with relative fluorescence intensity 3-10 times higher than in heart, liver, spleen, or kidney.
Reached maximum lung accumulation at 8 hours, accounting for 4.7% of the total administered amount (17.8 times higher than pirfenidone's lung accumulation).
Resulted in 100% mouse health over the 28-day period with no significant body weight loss.
Caused no histological damage in heart, liver, spleen, or kidney.
Chemical Information
-
No. CAS 3008320-14-4
-
Peso molecular 771.34
-
Fòrmula C34H30Cl6N4O4
-
SMILES
ClC1=CC(C(N2CCNC(C)C)=O)=C3C(C4=C(Cl)C=C3C2=O)=C1C5=C6C4=C(Cl)C=C(C(N(CCNC(C)C)C7=O)=O)C6=C7C=C5Cl.Cl.Cl
-
Envío
Room temperature in continental US; may vary elsewhere.
-
Almacenamiento
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureza y Documentación
Referencias
[1]. He KY, et al. High mobility group A1 (HMGA1) promotes esophageal squamous cell carcinoma progression by inhibiting STING-mediated anti-tumor immunity. Nature communications. 2025 Jun 02;16(1):5098. [Content Brief]
[2]. Liu Y, et al. Lung-Targeting Perylenediimide Nanocomposites for Efficient Therapy of Idiopathic Pulmonary Fibrosis. Nano letters. 2024 Oct 09;24(40):12701-12708. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
PDIC-DPC Related Classifications
HY-184535 Related Classifications
Powered by Bioz