Science

Understanding
cancer drug resistance

Resistance remains the major limiting factor to curing cancer. SCO-101 is designed to dismantle the mechanisms tumours use to evade treatment.

Cancer drug resistance

Why treatments stop working

Cancer drug resistance continues to be the major limiting factor to achieving cure for cancer patients. Our understanding of the underlying molecular and cellular mechanisms continues to develop with an ever-increasing number of new discoveries.

Intrinsic resistance

Resistance that is already there

Resistance may be an intrinsic property of some cells or clones within a tumour. Over time, under treatment with a cancer drug, these cells become enriched — until the entire tumour becomes resistant.

Acquired resistance

Resistance that develops

Tumour cells can also progress through a series of genetic events. As defects and changes accumulate, the cells eventually become resistant. Under continued treatment, only resistant cells remain — and the tumour becomes resistant.

Development of acquired and intrinsic resistance through clonal selection across cycles of drug treatment.

Publications

Scientific literature

Scientific Publications describing SCO-101 / Endovion

Four phase 1 trials to evaluate the safety and pharmacokinetic profile of single and repeated dosing of SCO-101 in adult male and female volunteers.

Bergmann TK et-al., Basic Clin Pharmacol Toxicol. 2020

Inhibition of ABCG2 by SCO-101 Enhances Chemotherapy Efficacy in Cancer.

Pfeiffer A et-al., Int J Mol Sci. 2025

PANTAX: a phase Ib clinical trial of the efflux pump inhibitor SCO-101 in combination with gemcitabine and nab-paclitaxel in non-resectable or metastatic pancreatic cancer.

Shim S et-al., Invest New Drugs. 2025

Pharmacodynamic modelling reveals synergistic interaction between docetaxel and SCO-101 in a docetaxel-resistant triple negative breast cancer cell line.

Nøhr-Nielsen A et-al., Eur J Pharm Sci. 2020

CDK12-inactivation-induced MYC signaling causes dependency on the splicing kinase SRPK1.

Liang J et-al., Mol Oncol. 2024

Chloride channel blockers inhibit iNOS expression and NO production in IFNgamma-stimulated microglial BV2 cells.

Kjaer K et-al., Brain Res. 2009

H-ras transformation sensitizes volume-activated anion channels and increases migratory activity of NIH3T3 fibroblasts.

Schneider L et-al., Pflugers Arch. 2008

Cell cycle-dependent activity of the volume- and Ca2+-activated anion currents in Ehrlich lettre ascites cells.

Klausen TK et-al., J Cell Physiol. 2007

SCO-101

A novel add-on that potentiates established therapy

Efflux Pharma's lead compound SCO-101 has a triple-acting mode of action and is used as a combination partner with anti-cancer drugs such as chemotherapy.

01 / Efflux pump

ABCG2

Drug efflux pump · stem-cell marker

Extracellular Cytoplasm

A potent inhibitor of the ABCG2 efflux pump and cancer stem-cell marker. Blocking it raises the intracellular concentration of cytotoxic chemotherapy — and cells with high ABCG2 are especially sensitive.

More drug inside → more cancer-cell death

02 / Enzyme

UGT1A1

Drug-metabolising liver enzyme

Independently of ABCG2, SCO-101 potently inhibits UGT1A1, which metabolises SN-38 — the active component of irinotecan — enhancing its plasma exposure and half-life in a modular fashion.

Longer SN-38 exposure & half-life

03 / Kinase

SRPK1

Serine / arginine-rich kinase

SCO-101 inhibits the kinase SRPK1, which is involved in endocrine-treatment resistance in cancer — addressing a third, distinct route of resistance.

Re-sensitises endocrine-resistant tumours