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^[1][2].

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 K_d 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 ESCC lung metastasis, 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 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.

771.34

C₃₄H₃₀Cl₆N₄O₄

3008320-14-4

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

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [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.

  [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.