Treatment with SZU305 (0.3-3 μM; 48 h) at a concentration of 3 μM for 48 h significantly induced almost complete degradation of RAD51 protein in human hepatocellular carcinoma cell line SK-HEP-1 [1]. After removal of SZU305 (3 μM; 48 h), the level of RAD51 protein in human hepatocellular carcinoma cell line SK-HEP-1 gradually recovered within 24 h, indicating that the turnover rate of RAD51 is relatively slow [1]. SZU305 (3 μM; 48 h) induced the degradation of RAD51 in human hepatocellular carcinoma cell line SK-HEP-1 through a CRBN and proteasome-dependent mechanism, which was dependent on ubiquitin modification and competitive binding to the catalytic site of RAD51 [1]. Treatment with SZU305 (0.5-10 μM; 72 h) for 72 hours showed concentration-dependent antiproliferative activity against human hepatocellular carcinoma cell line SK-HEP-1 [1]. SZU305 (1.25-10 μM; 12-14 days) can effectively inhibit the colony formation of human hepatocellular carcinoma cell line SK-HEP-1[1]. SZU305 (5-10 μM; 72 hours) can induce dose-dependent G2/M phase cell cycle arrest in human hepatocellular carcinoma cell line SK-HEP-1 after treatment at concentrations of 5 μM and 10 μM for 72 hours[1]. SZU305 (5-10 μM; 72 hours) can induce dose-dependent apoptosis in human hepatocellular carcinoma cell line SK-HEP-1[1]. SZU305 (3 μM; 48 hours) can selectively degrade RAD51 protein in SK-HEP-1 human hepatocellular carcinoma cells. After treatment at a concentration of 3 μM for 48 hours, the mRNA level of RAD51 protein did not change significantly, 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]. After 48 hours of treatment with SZU305, the homologous recombination repair efficiency of DR-U2OS reporter cells decreased, but had no significant effect on non-homologous end joining of EJ5-U2OS reporter cells[1]. When SZU305 was used in combination with 3 Gy ionizing radiation, it enhanced chromosome breaks in the SK-HEP-1 human hepatocellular carcinoma cell line, suggesting that its DNA damage repair function was impaired[1]. SZU305 inhibited the formation of γ-H2AX foci in the human hepatocellular carcinoma cell line SK-HEP-1, and this effect was enhanced when used in combination with VP16, CPT, sorafenib or IR, indicating that it disrupted the DNA damage response[1].

SZU305 (15 mg/kg; intravenous injection; once every other day for a total of 3 times) showed strong in vivo antitumor activity and low toxicity in the Huh-7 hepatocellular carcinoma xenograft mouse model [1].

Western Blot Analysis [1]
Cell Types: SK-HEP-1 human liver cancer cells
Tested Concentrations: 0.3 μM; 3 μM
Incubation Duration: 48 hours
Experimental Results: After 48 hours, the degradation rate of RAD51 at 3 μM concentration was approximately 99%.

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Western Blot Analysis [1]
Cell Types: SK-HEP-1 human liver cancer cells
Tested Concentrations: 3 μM
Incubation Duration: 48 hours (15b treatment); 0, 4, 8, 12, 24 hours (drug-free recovery)
Experimental Results: RAD51 protein expression gradually recovered within 24 hours after drug removal.

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Western Blot Analysis [1]
Cell Types: SK-HEP-1 human hepatocellular carcinoma cells
Tested Concentrations: 3 μM (15b treatment); MG132, MLN4924, pomalidomide, RI-1, 5a (pretreatment); siCRBN (pretreatment)
Incubation Duration: 48 h (15b treatment); 2 h (MG132, MLN4924, pomalidomide, RI-1, 5a pretreatment); 48 h (siCRBN pretreatment)
Experimental Results: Co-incubation with MG132 completely inhibited the degradation of RAD51. Studies have shown that MLN4924, pomalidomide, RI-1, 5a and siCRBN can prevent or reduce the degradation of RAD51.

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Cell viability assay [1]
Cell Types: SK-HEP-1 human liver cancer cells
Tested Concentrations: 0.5, 1, 2.5, 5, 10 μM
Incubation Duration: 72 hours
Experimental Results: SK-HEP-1 cell proliferation was inhibited in a concentration-dependent manner, and cell viability was reduced at all test concentrations.

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Animal/Disease Models:BALB/c nude mice (4-6 weeks old) [1]
Doses: 15 mg/kg
Route of Administration: Intravenous injection; once every other day for a total of 3 times
Experimental Results: Inhibited tumor growth, with a tumor/cell ratio (T/C ratio) of 75.6%. When used in combination with sorafenib, the T/C ratio was 16.7%. When used in combination with 3 Gy radiotherapy, the T/C ratio was 2.3%. No weight loss was observed, indicating low toxicity. Induced RAD51 degradation in tumor tissue. Reduced the expression of RAD51 and Ki67 in tumor tissue. Increased the level of cleaved caspase-3 in tumor tissue, with better results when used in combination with sorafenib or radiotherapy.

[1]. Development of Novel PROTAC RAD51 Degraders as Enhancers of DNA Damage Response for Hepatocellular Carcinoma Treatment. J Med Chem. 2026;69(4):3957-3983.

C32H28CL3FN6O6

717.96

Typically exists as solids at room temperature

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

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)