FOLH1 Knockout Cell Line (HEK 293)

The choice depends on whether you are studying FOLH1 (PSMA, prostate-specific membrane antigen, GCPII)'s role as a folate hydrolase/glutamate carboxypeptidase or modeling its applications in prostate cancer PET imaging and radioligand therapy. The Knockout line is the standard tool for asking whether PSMA is required for these processes — FOLH1 (PSMA) is a type II transmembrane glycoprotein with extracellular folate hydrolase and N-acetylated α-linked acidic dipeptidase (NAALADase) activity; PSMA is highly overexpressed in prostate cancer cells and is the molecular target of all clinical PSMA-PET imaging and radioligand therapy. Overexpression is useful for studying PSMA in heterologous expression contexts. For prostate cancer therapeutic research, the EDITGENE FOLH1 Knockout in HEK293 is uniquely valuable — HEK293 supports systematic PSMA-targeted compound development. Rescue with wild-type or enzymatically-dead PSMA enables structure-function studies. The knockout is a critical specificity control for ⭐⭐ Lu-177-PSMA-617 (lutetium-177-vipivotide tetraxetan, Pluvicto/Novartis, FDA-approved 2022 for metastatic castration-resistant prostate cancer), Lu-177-PSMA-I&T, and emerging PSMA-targeted radioligand therapies including diagnostics (68Ga-PSMA-11/Locametz, F-18-DCFPyL/Pylarify for PSMA-PET) and therapeutics.

Primary applications: • PSMA radioligand therapy specificity: critical genetic control for Lu-177-PSMA-617 (Pluvicto, FDA-approved for mCRPC), Lu-177-PSMA-I&T — these therapies should have no effect in FOLH1-null cells. • PSMA-PET imaging tracer development: 68Ga-PSMA-11 (Locametz), F-18-DCFPyL (Pylarify), 68Ga-PSMA-617 specificity testing. • PSMA-targeted ADC/CAR-T validation: anti-PSMA antibody-drug conjugates and CAR-T cells specificity control. • Folate hydrolase activity: NAALADase activity and folate hydrolysis assays in FOLH1-null cells. EDITGENE recommends this model as the gold-standard genetic specificity control for PSMA-targeted prostate cancer radioligand therapy and diagnostic imaging development.

Yes. PSMA rescue experiments are well-established for prostate cancer therapeutic research: • Construct design: use a codon-modified FOLH1 sequence with a small intracellular C-terminal tag (FLAG, HA). PSMA is a type II transmembrane glycoprotein — N-terminal short cytoplasmic tail, single transmembrane span, large extracellular catalytic domain with C-terminal exopeptidase activity — preserve membrane topology. • Surface localization validation: confirm plasma membrane localization by cell surface staining before PSMA-targeted compound testing. • Enzymatically-dead rescue: catalytic glutamate mutations abolish folate hydrolase/NAALADase activity. • Functional readout: rescue should restore PSMA-targeted compound (Lu-177-PSMA-617, 68Ga-PSMA-11) cellular binding and uptake. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation.