2. PROTAC Cell Cycle/DNA Damage Apoptosis Immunology/Inflammation
  3. PROTACs RAD51 DNA/RNA Synthesis Apoptosis IKZF Family
  4. SZU305

SZU305 is a RAD51 PROTAC degrader, with DC50 values of 307.45 nM and 84.19 nM in SK-HEP-1 and Huh-7 cells, respectively. SZU305 inhibits DNA damage repair, induces cell cycle arrest and apoptosis. SZU305 moderately reduces the protein levels of IKZF1 and IKZF3 at high concentrations. SZU305 can be used in studies related to hepatocellular carcinoma.
(Pink: RAD51 ligand (HY-167881); Blue: Cereblon ligand (HY-W087383); Black: linker).

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SZU305

SZU305 Chemical Structure

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SZU305 Related Antibodies

Top Publications Citing Use of Products

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von Hippel-Lindau (VHL) Cereblon MDM2 cIAP1

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RNASE L DNA Polymerases RNA Polymerases Helicases DNA Ligase

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IKZF1 IKZF2 IKZF3 IKZF4

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Description

SZU305 is a RAD51 PROTAC degrader, with DC50 values of 307.45 nM and 84.19 nM in SK-HEP-1 and Huh-7 cells, respectively. SZU305 inhibits DNA damage repair, induces cell cycle arrest and apoptosis. SZU305 moderately reduces the protein levels of IKZF1 and IKZF3 at high concentrations. SZU305 can be used in studies related to hepatocellular carcinoma[1]. (Pink: RAD51 ligand (HY-167881); Blue: Cereblon ligand (HY-W087383); Black: linker).

IC50 & Target[1]

Cereblon

 

IKZF1

 

IKZF3

 

In Vitro

SZU305 (0.3-3 μM; 48 h) potently induces nearly complete degradation of RAD51 in human hepatocellular carcinoma cells SK-HEP-1 following treatment with 3 μM for 48 h[1].
Removal of SZU305 (3 μM; 48 h) causes a gradual recovery of RAD51 protein levels within 24 h in human hepatocellular carcinoma SK-HEP-1 cells, indicating that the turnover rate of RAD51 is relatively slow[1].
SZU305 (3 μM; 48 h) induces RAD51 degradation in the human hepatocellular carcinoma cell line SK-HEP-1 via a CRBN- and proteasome-dependent mechanism, and this degradation process relies on ubiquitin-like modification and competitive binding to the catalytic site of RAD51[1].
SZU305 (0.5-10 μM; 72 h) exerts concentration-dependent antiproliferative activity against human hepatocellular carcinoma cell line SK-HEP-1 after 72 h of treatment[1].
SZU305 (1.25-10 μM; 12-14 days) potently inhibits colony formation of human hepatocellular carcinoma cell line SK-HEP-1[1].
SZU305 (5-10 μM; 72 h) induces dose-dependent G2/M cell cycle arrest in human hepatocellular carcinoma SK-HEP-1 cells following 72 h of treatment at concentrations of 5 μM and 10 μM[1].
Treatment with SZU305 (5-10 μM; 72 h) induces dose-dependent apoptosis in human hepatocellular carcinoma cell line SK-HEP-1[1].
SZU305 (3 μM; 48 h) selectively degrades the RAD51 protein in SK-HEP-1 human hepatocellular carcinoma cells, without significantly altering its mRNA level after 48 h of treatment at 3 μM, while regulating the expression of genes and proteins involved in DNA damage repair, apoptosis and stress response[1].
SZU305 (3 μM; 48 h) enhances DNA damage in SK-HEP-1 human hepatocellular carcinoma cells[1].
Treatment of DR-U2OS reporter cells with SZU305 for 48 h impairs their homologous recombination repair efficiency, but exerts no significant effect on non-homologous end joining in EJ5-U2OS reporter cells[1].
SZU305 enhances chromosome breakage in the human hepatocellular carcinoma cell line SK-HEP-1 when combined with 3 Gy IR, suggesting impaired DNA damage repair function[1].
SZU305 impairs the formation of γ-H2AX foci in the human hepatocellular carcinoma cell line SK-HEP-1, and this effect is enhanced when combined with VP16, CPT, sorafenib or IR, suggesting that it disrupts the DNA damage response[1].

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

SZU305 Related Antibodies

Western Blot Analysis[1]

Cell Line: SK-HEP-1 human liver cancer cells
Concentration: 0.3 μM; 3 μM
Incubation Time: 48 h
Result: Induced ~99% RAD51 degradation at 3 μM after 48 h.

Western Blot Analysis[1]

Cell Line: SK-HEP-1 human liver cancer cells
Concentration: 3 μM
Incubation Time: 48 h (15b treatment); 0, 4, 8, 12, 24 h (drug-free recovery)
Result: Allowed RAD51 protein expression to gradually recover within 24 h after removal.

Western Blot Analysis[1]

Cell Line: SK-HEP-1 human liver cancer cells
Concentration: 3 μM (15b treatment); MG132, MLN4924, pomalidomide, RI-1, 5a (pretreatment); siCRBN (pretreatment)
Incubation Time: 48 h (15b treatment); 2 h (MG132, MLN4924, pomalidomide, RI-1, 5a pretreatment); 48 h (siCRBN pretreatment)
Result: Had RAD51 degradation completely abolished by co-incubation with MG132.
Showed RAD51 degradation prevented or diminished by MLN4924, pomalidomide, RI-1, 5a, and siCRBN.

Cell Viability Assay[1]

Cell Line: SK-HEP-1 human liver cancer cells
Concentration: 0.5, 1, 2.5, 5, 10 μM
Incubation Time: 72 h
Result: Inhibited SK-HEP-1 cell proliferation in a concentration-dependent manner, with reduced cell viability observed at all tested concentrations.

Cell Proliferation Assay[1]

Cell Line: SK-HEP-1 human liver cancer cells
Concentration: 1.25, 2.5, 5 and 10 μM
Incubation Time: 12-14 days
Result: Suppressed colony formation more effectively than RI-1 at equivalent concentrations.

Cell Cycle Analysis[1]

Cell Line: SK-HEP-1 human liver cancer cells
Concentration: 5 μM; 10 μM
Incubation Time: 72 h
Result: Induced dose-dependent cell cycle arrest at the G2/M phase, with G1 phase population reduced from 80.15% (control) to 50.07% (5 μM) and 46.36% (10 μM), while G2/M phase population increased from 12.49% (control) to 34.63% (5 μM) and 38.42% (10 μM).

Apoptosis Analysis[1]

Cell Line: SK-HEP-1 human liver cancer cells
Concentration: 5 μM; 10 μM
Incubation Time: 72 h
Result: Induced dose-dependent apoptosis, with up to ~23% apoptotic cells observed at 10 μM.
In Vivo

SZU305 (15 mg/kg; i.v.; once every other day, 3 doses total) exhibits potent in vivo anti-tumor activity with low toxicity in the Huh-7 hepatocellular carcinoma xenograft mouse model[1].

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

Animal Model: BALB/c nude (4-6 weeks old)[1]
Dosage: 15 mg/kg
Administration: i.v.; once every other day, 3 doses total
Result: Suppressed tumor growth with a T/C ratio of 75.6%.
Combined with sorafenib, achieved a T/C ratio of 16.7%.
Combined with 3 Gy irradiation, achieved a T/C ratio of 2.3%.
Caused no body weight loss, indicating low toxicity.
Induced RAD51 degradation in tumor tissue.
Reduced RAD51 and Ki67 expression in tumor tissue.
Elevated cleaved caspase-3 levels in tumor tissue, with greater effects seen in combination with sorafenib or irradiation.
Molecular Weight

717.96

Formula

C32H28Cl3FN6O6
SMILES

O=C1N(C(C2=C1C=C(C(N3CC(CC3)CN4CCN(C5=C(C(N(C5=O)C6=CC=C(C(Cl)=C6)Cl)=O)Cl)CC4)=C2)F)=O)C7C(NC(CC7)=O)=O
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Purity & Documentation
References
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Keywords:

SZU305SZU 305SZU-305PROTACsRAD51DNA/RNA SynthesisApoptosisIKZF FamilyIkaros zinc finger protein familyhepatocellular carcinomaSK-HEP-1Huh-7proteasomeliver cancer cellshomologous recombination DNA repairCRBNIKZF3IKZF1Inhibitorinhibitorinhibit

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