AZD5335
AZD5335 is an ADC targeting FRα, with an IC50 of 10.6 nM against human FRα. AZD5335 specifically binds to FRα, mediates internalization and trafficking to lysosomal compartments, while delivering a topoisomerase I inhibitor payload that traps TOP1-DNA cleavage complexes. AZD5335 induces DNA damage response via the ATR, ATM, Chk1 and Chk2 signaling pathways, and increases the levels of phosphorylated KAP1, phosphorylated RPA, phosphorylated γH2AX, as well as PARP cleavage. AZD5335 exhibits bystander cytotoxicity against FRα-negative cells co-cultured with FRα-expressing cells. AZD5335 induces potent and durable responses and complete regression in ovarian cancer models, including models with low FRα expression and models resistant to Elahere, with enhanced efficacy when combined with Carboplatin, Bevacizumab or poly (ADP-ribose) polymerase inhibitors. AZD5335 can be used for ovarian cancer research.
For research use only. We do not sell to patients.
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
FR-α 10.6 nM (IC50) |
Chk1 |
Chk2 |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| KB | IC50 |
0.5270 nM
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Cytotoxicity against FRα-expressing KB cancer cells assessed as reduction in cell viability incubated for 6 days by CellTiter-Glo (CTG) 2.0 assay.
Cytotoxicity against FRα-expressing KB cancer cells assessed as reduction in cell viability incubated for 6 days by CellTiter-Glo (CTG) 2.0 assay.
|
41091103 |
| JEG-3 | IC50 |
2.091 nM
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Cytotoxicity against FRα-expressing Jeg-3 cancer cells assessed as reduction in cell viability incubated for 6 days by CellTiter-Glo (CTG) 2.0 assay.
Cytotoxicity against FRα-expressing Jeg-3 cancer cells assessed as reduction in cell viability incubated for 6 days by CellTiter-Glo (CTG) 2.0 assay.
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41091103 |
| IGROV-1 | IC50 |
5.284 nM
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Cytotoxicity against FRα-expressing IGROV-1 cancer cells assessed as reduction in cell viability incubated for 6 days by CellTiter-Glo (CTG) 2.0 assay.
Cytotoxicity against FRα-expressing IGROV-1 cancer cells assessed as reduction in cell viability incubated for 6 days by CellTiter-Glo (CTG) 2.0 assay.
|
41091103 |
In Vitro
AZD5335 (0.001707-666.66 nM; 6 days) potently reduces the viability of FRα-expressing KB, Jeg-3 and IGROV-1 cancer cells in vitro, with IC50 values of 0.5270 nM, 2.091 nM and 5.284 nM, respectively[1].
AZD5335 (0-300 nM; 6 days) exhibits bystander cytotoxicity and reduces the survival rate of FRα-negative lucKB_FRα-KO cells when co-cultured with FRα-expressing KB cells[1].
AZD5335 (0.104-30 µg/mL; 6 days) exhibits synergistic cytotoxic activity with Carboplatin (HY-17393) and Saruparib (HY-132167) in FRα-expressing KB, Jeg-3 and IGROV-1 cancer cells[1].
AZD5335 (66.7 nM; 24-72 h) activates the DNA damage response pathway in FRα-expressing KB cancer cells, which is consistent with the mechanism of action of its TOP1i payload[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:FRα-expressing KB, Jeg-3, and IGROV-1 cancer cell lines
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Concentration:0.001707-666.66 nM
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Incubation Time:6 days
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Result:Reduced cell viability in all three FRα-expressing cell lines.
Inhibited KB cell viability with an IC50 of 0.5270 nM.
Inhibited Jeg-3 cell viability with an IC50 of 2.091 nM.
Inhibited IGROV-1 cell viability with an IC50 of 5.284 nM.
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Cell Line:FRα-expressing KB, Jeg-3, and IGROV-1 cancer cell lines
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Concentration:0.104-30 µg/mL
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Incubation Time:6 days
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Result:Enhanced cytotoxicity across all three cell lines when combined with Carboplatin compared to monotherapy, with HSA synergy scores of 30.24 (Jeg-3), 4.218 (KB), and 2.339 (IGROV-1).
Yielded minimal to no added benefit when combined with Bevacizumab, with low HSA synergy scores.\nEnhanced cytotoxicity across all three cell lines when combined with saruparib compared to either single agent alone, with HSA synergy scores of 40.76 (Jeg-3), 23.81 (KB), and 7.348 (IGROV-1).
In Vivo
AZD5335 (1.25-5 mg/kg; intravenous injection; single administration) induces 53.37% tumor growth inhibition in FRα-low expressing SKOV-3 ovarian cancer xenografts at a single intravenous dose of 5 mg/kg[1].
AZD5335 (2.5-5 mg/kg; intravenous injection; single dose) induces an overall response rate of 82% at a single intravenous dose of 2.5 mg/kg and 76% at a single intravenous dose of 5 mg/kg in a panel of ovarian cancer patient-derived xenograft models with varying FRα expression levels[1].
AZD5335 (2.5-5 mg/kg; intravenous injection; single administration) induces significant and persistent tumor growth inhibition in Elahere-intolerant ovarian cancer xenograft models[1].
AZD5335 (intravenous injection; single dose, 2.5 mg/kg) induces 85.96% tumor growth inhibition in FRα-low-expressing OV90 ovarian cancer xenograft models; its efficacy is enhanced when combined with Bevacizumab (HY-P9906), Carboplatin, or both, with a maximum TGI of up to 98.66%[1].
AZD5335 (1.25-2.5 mg/kg, intravenous injection, single dose; or in combination with a 1 mg/kg poly (ADP-ribose) polymerase inhibitor administered orally daily for 28 days) enhances tumor growth inhibition when combined with the poly (ADP-ribose) polymerase inhibitor in low/very low FRα ovarian cancer xenograft models [1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:CB-17 SCID (female, ovarian cancer KB cell-derived subcutaneous xenografts)[1]
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Dosage:1.25 mg/kg; 2.5 mg/kg; 5 mg/kg
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Administration:i.v.; single dose
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Result:Induced complete and durable tumor regression with 100% tumor growth inhibition (TGI) at 5 mg/kg.
Resulted in 55.17% TGI at 2.5 mg/kg.
Resulted in 78.38% TGI at 1.25 mg/kg.
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Animal Model:CB-17 SCID (female, ovarian cancer IGROV-1 cell-derived subcutaneous xenografts)[1]
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Dosage:1.25 mg/kg; 2.5 mg/kg; 5 mg/kg
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Administration:i.v.; single dose
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Result:Resulted in 95.55% TGI at 5 mg/kg.
Resulted in 86.75% TGI at 2.5 mg/kg.
Resulted in 43.8% TGI at 1.25 mg/kg.
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Animal Model:NOD/SCID gamma (NSG) (female, ovarian cancer OVCAR-3 cell-derived subcutaneous xenografts)[1]
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Dosage:1.25 mg/kg; 2.5 mg/kg; 5 mg/kg
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Administration:i.v.; single dose
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Result:Resulted in greater than 80% TGI across all tested doses.
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Animal Model:NOD/SCID gamma (NSG) (female, ovarian cancer SKOV-3 cell-derived subcutaneous xenografts)[1]
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Dosage:1.25 mg/kg; 2.5 mg/kg; 5 mg/kg
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Administration:i.v.; single dose
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Result:Resulted in 53.37% TGI.
Induced dose-dependent reductions in TGI at lower doses, with only the 5 mg/kg dose showing significant activity.
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Animal Model:NOD/SCID gamma (NSG) (female, ovarian cancer patient-derived subcutaneous xenografts with variable FRα expression)[1]
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Dosage:2.5 mg/kg; 5 mg/kg
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Administration:i.v.; single dose
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Result:Resulted in an 82% overall response rate, with 14 of 17 models exhibiting a tumor volume reduction of 30% or greater, including 4 of 4 FRα-high models, 10 of 11 FRα-low models, and 0 of 2 FRα-ultra-low models.
Resulted in a 76% overall response rate, with 13 of 17 models exhibiting a tumor volume reduction of 30% or greater, including 4 of 4 FRα-high models, 9 of 11 FRα-low models, and 0 of 2 FRα-ultra-low models, with deeper, dose-dependent responses observed compared to the 2.5 mg/kg dose.
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Animal Model:NOD/SCID gamma (NSG) (female, Elahere-ineligible ovarian cancer xenografts: CTG-3226 PDX, OV0857-CIS PDX, OVCAR-3 CDX)[1]
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Dosage:2.5 mg/kg; 5 mg/kg
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Administration:i.v.; single dose
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Result:Demonstrated significant tumor growth inhibition associated with durable responses in all three Elahere-ineligible models.
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Animal Model:NOD/SCID gamma (NSG) (female, ovarian cancer OV90 cell-derived subcutaneous xenografts, FRα-low)[1]
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Dosage:2.5 mg/kg (monotherapy; combination with Bevacizumab; combination with Carboplatin; combination with Bevacizumab and Carboplatin)
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Administration:i.v.; single dose; monotherapy or in combination with 5 mg/kg bevacizumab i.p. single dose, 100 mg/kg carboplatin i.p. single dose, or both
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Result:Resulted in 85.96% TGI as monotherapy.
Resulted in 98.66% TGI when combined with Bevacizumab.
Resulted in 96.38% TGI when combined with Carboplatin.
Resulted in 98.63% TGI when combined with Bevacizumab and carboplatin.
Showed enhanced efficacy with all combination treatments compared to monotherapy.
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Animal Model:NOD/SCID gamma (NSG) (female, ovarian cancer OVCAR-3 CDX, OV2022F PDX, CTG-3783 PDX, low/ultra-low FRα expression)[1]
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Dosage:1.25 mg/kg (OVCAR-3, OV2022F models; monotherapy or combination); 2.5 mg/kg (CTG-3783 model; monotherapy or combination)
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Administration:i.v.; single dose; monotherapy or in combination with 1 mg/kg poly(ADP-ribose) polymerase inhibitor p.o. daily for 28 days
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Result:Resulted in 86.14% TGI as monotherapy and 92.83% TGI in combination with poly(ADP-ribose) polymerase inhibitor in OVCAR-3.
Resulted in 53.91% TGI as monotherapy and 97.15% TGI in combination with poly(ADP-ribose) polymerase inhibitor in OV2022F.
Resulted in 72.82% TGI as monotherapy and 95.49% TGI in combination with poly(ADP-ribose) polymerase inhibitor in CTG-3783.
Showed enhanced efficacy with all combination treatments compared to monotherapy.
Chemical Information
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SMILES
[AZD5335]
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Mammalian live/dead viability and cytotoxicity staining
Live/dead viability and cytotoxicity staining assays are based on the simultaneous detection of intracellular esterase activity in metabolically active (viable) cells and membrane integrity loss in non-viable cells. In commonly used dual-staining approaches, membrane-permeant fluorogenic substrates are converted by intracellular esterases into fluorescent products in live cells, while impermeant DNA-binding dyes selectively enter cells with compromised plasma membranes and label nucleic acids in dead or dying cells, enabling discrimination between viable and non-viable populations by fluorescence microscopy or flow cytometry.
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Lysosome and acidic-vesicle live-cell staining
Lysosome and acidic-vesicle live-cell staining detects acidic intracellular compartments by using membrane-permeant acidotropic probes that accumulate in low-pH vesicles, including lysosomes, late endosomes, autolysosomes, and acidic phagosomes. LysoTracker staining is commonly used as an intensity-based readout of acidic lysosomal compartment abundance or enlargement, while acridine orange produces green fluorescence in less concentrated compartments and red fluorescence after concentration-dependent accumulation in acidic vesicular organelles. Loss or reduction of acridine-orange red signal can be used as a readout of lysosomal membrane permeabilization or reduced acidic-vesicle integrity. This protocol is designed for live cultured cells and can be adapted for fluorescence microscopy, high-content imaging, plate-reader readout, or flow cytometry when the selected literature supports the readout. Because these dyes report acidotropic accumulation rather than lysosome identity alone,
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Genotoxicity/Mutagenicity Study
The bacterial reverse mutation assay detects point mutations that restore amino-acid prototrophy in auxotrophic Salmonella typhimurium or Escherichia coli tester strains; after exposure to a test article, mutagenic activity is read out as an increased number of revertant colonies on minimal agar compared with the vehicle control. The assay uses tester strains with different mutation targets so that base-substitution and frameshift mutagens can be detected, and testing is performed with and without exogenous mammalian metabolic activation because some chemicals require biotransformation to become mutagenic.
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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)