Biological Activity

Bioactivity / Mechanism

Abiraterone binds CYP17A1 through coordination of its pyridyl nitrogen to the heme iron; its 3β-hydroxyl group interacts with Asn202. Kinetic experiments support a two-step, slow-binding mechanism, with final-complex Ki* values of 0.39 nM for the hydroxylase readout and 0.42 nM for the lyase readout. These fitted constants differ from initial-binding and IC50 measurements. [1,2]

Abiraterone also inhibits CYP17A1 hydroxylase reactions: IC50 values were 76 ± 5 nM for progesterone and 121 ± 7 nM for pregnenolone hydroxylation in one reconstituted system (mean ± S.E., two independent experiments). Potency depends on substrate and assay conditions. [3]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target	Activity	Value
CYP17 (Cell-free assay)		2 nM

Cellular Effect

Cell Line	Activity	Value	Description	Reference
A549	IC50	35.8 nM	Inhibition of recombinant human CYP17 expressed in human A549 cell membranes using 17-alpha hydroxyprogesterone as substrate and NADPH as cofactor pretreated for 5 mins followed by substrate and cofactor addition after 60 mins by LC/MS analysis	[PMID: 28350999]
A549	GI50	95 μM	Antiproliferative activity against human A549 cells after 48 hrs by SRB assay	[PMID: 29172080]
DU-145	GI50	> 10 μM	Antiproliferative activity against human DU-145 cells assessed as cell growth inhibition incubated for 48 hrs by MTT assay	[PMID: 34908406]
ECa-109 cell line	IC50	> 32 μM	Antiproliferative activity against human EC109 cells after 72 hrs by MTT assay	[PMID: 29310026]
GES1	IC50	13.12 μM	Antiproliferative activity against human GES-1 cells after 72 hrs by MTT assay	[PMID: 29310026]
HBL-100	GI50	> 100 μM	Antiproliferative activity against human HBL100 cells after 48 hrs by SRB assay	[PMID: 29172080]
HEK-293T	IC50	> 100 μM	Cytotoxicity against HEK293T cells assessed as inhibition of cell growth incubated for 72 hrs by MTT assay	[PMID: 36455509]
HeLa	IC50	16.9 μM	Antiproliferative activity against human HeLa cells assessed as inhibition of cell growth incubated for 72 hrs by MTT assay	[PMID: 36455509]
HeLa	GI50	7.9 μM	Antiproliferative activity against human HeLa cells after 48 hrs by SRB assay	[PMID: 29172080]
HepG2	IC50	59.8 μM	Antiproliferative activity against human HepG2 cells assessed as inhibition of cell growth incubated for 72 hrs by MTT assay	[PMID: 36455509]
hTERT-BJ	GI50	4.5 μM	Cytotoxicity against human hTERT-BJ cells assessed as cell growth inhibition after 48 hrs SRB assay	[PMID: 29172080]
LNCaP	IC50	2706 nM	Antiproliferative activity against human LNCAP cells assessed as reduction in cell viability measured after 6 days by CellTiter-Glo assay	[PMID: 36070471]
LNCaP	IC50	3.29 μM	Antiproliferative activity against human LNCAP cells after 72 hrs by MTT assay	[PMID: 29310026]
LNCaP	IC50	800 nM	In vitro cytochrome P450 17A1 inhibition was assayed using the rapid acetic acid releasing assay (AARA), utilizing intact P450c17-expressing Escherichia coli or P450c17-LNCaP cells as the enzyme source.	[PMID: 12773039]
MCF7	IC50	19.3 μM	Growth inhibition of human MCF7 cells after 72 hrs by MTT assay	[PMID: 27209562]
MCF7	IC50	38.2 μM	Antiproliferative activity against human MCF7 cells assessed as inhibition of cell growth incubated for 72 hrs by MTT assay	[PMID: 36455509]
MDA-MB-231	IC50	19.2 μM	Growth inhibition of human MDA-MB-231 cells after 72 hrs by MTT assay	[PMID: 27209562]
MDA-MB-361	IC50	20.4 μM	Growth inhibition of human MDA-MB-361 cells after 72 hrs by MTT assay	[PMID: 27209562]
MGC-803	IC50	7.72 μM	Antiproliferative activity against human MGC803 cells after 72 hrs by MTT assay	[PMID: 29310026]
PC-3	GI50	> 10 μM	Antiproliferative activity against human PC-3 cells assessed as cell growth inhibition incubated for 48 hrs by MTT assay	[PMID: 34908406]

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In Vitro Studies

In VCaP cells, a 2-hour exposure to 40 μM abiraterone followed by washout left DHEA production more suppressed than after the ketoconazole comparator through 60 minutes. This demonstrates persistent steroidogenesis inhibition under the tested conditions; it is not a proliferation assay. [2]

CYP17A1 binding structure

Biochemical assay · Purified, N-terminally modified human CYP17A1 expressed in E. coli; abiraterone complex (PDB 3RUK). [1]

The pyridyl nitrogen coordinates the heme iron, while the 3β-hydroxyl group interacts with Asn202. The steroid core lies about 60° above the heme plane.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
CYP17A1–abiraterone crystal structure	Resolution 2.6 Å	[1]

Literature-Reported Treatment Conditions

Treatment concentration: 10 μM abiraterone in crystallization protein buffer
Method: Hanging-drop vapor diffusion at 20°C; protein 30 mg/mL.
Reported limits: Crystal-growth duration not specified in the reviewed methods. Crystallization conditions are not a cellular dosing recommendation.

Methods and source locations

Compound reported in the paper: Abiraterone; Compound label in the paper: Abiraterone

Applies to the reported abiraterone experiment; acetate and metabolite results are not assigned to this product.

Methods: Synthesis and characterization of abiraterone; Crystallization and structure determination; structural results, Figure 2b–c.

CYP17A1–abiraterone crystal structure: X-ray crystallography; structural result stated in main text and binding pose inspected in Figure 2. — Methods: Synthesis and characterization of abiraterone; Crystallization and structure determination; structural results, Figure 2b–c.

Inhibition of CYP17A1 hydroxylase reactions

Biochemical assay · Purified human CYP17A1 (100 nM) with human NADPH-cytochrome P450 reductase (1:4 molar ratio). [3]

Abiraterone inhibited hydroxylation of both progesterone and pregnenolone in a defined reconstituted enzyme system.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Progesterone 17α-hydroxylation inhibition	IC50 76 ± 5 nM	[3]
Pregnenolone 17α-hydroxylation inhibition	IC50 121 ± 7 nM	[3]

Literature-Reported Treatment Conditions

Treatment concentration: 0–30 μM inhibitor for progesterone hydroxylation; 0–60 μM for pregnenolone hydroxylation (assay ranges reported for the inhibitor panel).
Exposure duration: 20 minutes at 37°C
Method: NADPH-initiated reactions, 500 μL; substrates 10 μM progesterone or 1 μM pregnenolone.
Reported limits: Inhibitor solvent and preincubation interval are not specified in the reviewed assay paragraph.

Methods and source locations

Compound reported in the paper: Abiraterone; Compound label in the paper: Abiraterone

Applies to the reported abiraterone experiment; acetate and metabolite results are not assigned to this product.

Materials; Enzyme Inhibition Assays; Table 3, abiraterone row and footnote; Results: Inhibition of Off-Target Progesterone and Pregnenolone Hydroxylation Reactions.

Progesterone 17α-hydroxylation inhibition: HPLC/UV-visible quantification; mean ± S.E. from two independent experiments; duplicate or triplicate concentrations within each experiment. — Materials; Enzyme Inhibition Assays; Table 3, abiraterone row and footnote; Results: Inhibition of Off-Target Progesterone and Pregnenolone Hydroxylation Reactions.

Pregnenolone 17α-hydroxylation inhibition: GC/MS of silylated product; mean ± S.E. from two independent experiments; duplicate or triplicate concentrations within each experiment. — Materials; Enzyme Inhibition Assays; Table 3, abiraterone row and footnote; Results: Inhibition of Off-Target Progesterone and Pregnenolone Hydroxylation Reactions.

Time-dependent CYP17A1 inhibition

Biochemical assay · Recombinant human CYP17A1 bactosomes with reductase and cytochrome b5; enzyme 5 pmol/mL. [2]

Preincubation-dependent inhibition supported a two-step, slow-binding model. Final-complex inhibition constants and calculated dissociation half-lives differed from initial-complex parameters.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Initial encounter complex, hydroxylase readout	Ki,app 132 ± 2.02 nM	[2]
Initial encounter complex, lyase readout	Ki,app 118 ± 1.13 nM	[2]
Final high-affinity complex, hydroxylase readout	Ki* 0.39 nM	[2]
Final high-affinity complex, lyase readout	Ki* 0.42 nM	[2]
Hydroxylase-based complex dissociation	Dissociation t1/2 42.0 h	[2]
Lyase-based complex dissociation	Dissociation t1/2 30.1 h	[2]

Literature-Reported Treatment Conditions

Treatment concentration: 5–100 nM for preincubation experiments; 1–300 nM for initial-velocity experiments.
Exposure duration: 0–30 minutes preincubation at 37°C; 20-minute reaction.
Method: 50 μM progesterone or 5 μM 17α-hydroxypregnenolone; LC/MS/MS product measurement; triplicate incubations.
Reported limits: Inhibitor solvent is not specified in the reviewed biochemical methods.

Methods and source locations

Compound reported in the paper: Abiraterone; Compound label in the paper: Abiraterone

Applies to the reported abiraterone experiment; acetate and metabolite results are not assigned to this product.

Methods: Slow-Binding Inhibition Kinetics, Estimation of Ki,app and Determination of Ki*; Results, Figures 2–3 and Table 1 (abiraterone rows).

Initial encounter complex, hydroxylase readout: Initial-velocity fit; mean ± S.D., triplicate determinations. — Methods: Slow-Binding Inhibition Kinetics, Estimation of Ki,app and Determination of Ki*; Results, Figures 2–3 and Table 1 (abiraterone rows).

Initial encounter complex, lyase readout: Initial-velocity fit; mean ± S.D., triplicate determinations. — Methods: Slow-Binding Inhibition Kinetics, Estimation of Ki,app and Determination of Ki*; Results, Figures 2–3 and Table 1 (abiraterone rows).

Final high-affinity complex, hydroxylase readout: Calculated using two-step kinetic model; no uncertainty supplied for this table value. — Methods: Slow-Binding Inhibition Kinetics, Estimation of Ki,app and Determination of Ki*; Results, Figures 2–3 and Table 1 (abiraterone rows).

Final high-affinity complex, lyase readout: Calculated using two-step kinetic model; no uncertainty supplied for this table value. — Methods: Slow-Binding Inhibition Kinetics, Estimation of Ki,app and Determination of Ki*; Results, Figures 2–3 and Table 1 (abiraterone rows).

Hydroxylase-based complex dissociation: Calculated from reverse isomerization rate; assumes this step limits reactivation. — Methods: Slow-Binding Inhibition Kinetics, Estimation of Ki,app and Determination of Ki*; Results, Figures 2–3 and Table 1 (abiraterone rows).

Lyase-based complex dissociation: Calculated from reverse isomerization rate; assumes this step limits reactivation. — Methods: Slow-Binding Inhibition Kinetics, Estimation of Ki,app and Determination of Ki*; Results, Figures 2–3 and Table 1 (abiraterone rows).

VCaP steroidogenesis and recovery after washout

Cell-based study · Human VCaP prostate cancer cells, passages 8–16; 0.4 million cells/well in 24-well plates. [2]

Abiraterone reduced DHEA formation during coincubation and maintained suppression after removal. Recovery remained lower than with the ketoconazole comparator through the 60-minute washout interval.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
DHEA production after inhibitor removal	Functional recovery comparison Lower recovery with abiraterone at 0, 30 and 60 minutes; one-sided P = 0.0158, 0.0071 and 0.0281, respectively.	[2]

Literature-Reported Treatment Conditions

Treatment concentration: Coincubation: abiraterone 20 μM or ketoconazole 25 μM. Washout design: either inhibitor 40 μM.
Exposure duration: 2-hour inhibitor exposure; washout 0, 30 or 60 minutes; then 30-minute probe incubation.
Method: Probe substrate 17α-hydroxypregnenolone 30 μM; LC/MS/MS of DHEA oxime; separate inhibitor and vehicle-control arms.
Vehicle: Abiraterone: 0.5% v/v methanol for coincubation or 1% v/v methanol for preincubation; ketoconazole: corresponding DMSO vehicles. Probe solvent: 0.6% methanol for coincubation or 1% methanol after washout.
Co-treatment: Ketoconazole was a parallel comparator, not combined treatment.
Reported limits: Exact percentages are plotted but not numerically tabulated; no curve/bar values estimated.

Methods and source locations

Compound reported in the paper: Abiraterone; Compound label in the paper: Abiraterone

Applies to the reported abiraterone experiment; acetate and metabolite results are not assigned to this product.

Methods: Verifying the Functionality of the C17,20 Lyase Pathway in VCaP Cells and Functional Recovery Experiments; Results: Prolonged CYP17A1 Binding; Figure 5B–C and legend.

DHEA production after inhibitor removal: DHEA oxime relative to each vehicle control; unpaired one-tailed t tests; mean ± S.D. from at least three experiments with triplicate determinations. — Methods: Verifying the Functionality of the C17,20 Lyase Pathway in VCaP Cells and Functional Recovery Experiments; Results: Prolonged CYP17A1 Binding; Figure 5B–C and legend.

In Vivo Studies

In castrate mice with LuCaP23CR or LuCaP35CR xenografts, reported abiraterone treatment at 0.5 mmol/kg/d intraperitoneally for 21 days delayed progression to the tumor-size endpoint and suppressed intratumoral androgens. Median endpoint times increased from 14 to 24 days and from 17 to 39 days, respectively. Tumor recurrence persisted, and late LuCaP35CR samples showed testosterone recovery after treatment. [4]

Responses depended on the model and endpoint. In a separate LAPC-4 xenograft experiment, free abiraterone at 0.15 mmol/kg subcutaneously twice daily for 31 days did not significantly reduce androgen-sensitive organ weights or tumor AR protein. These pharmacodynamic findings do not establish absence of an antitumor effect. [5]

LuCaP xenograft growth and intratumoral androgen response

Animal study · Castrate male CB-17 SCID mice bearing LuCaP23CR or LuCaP35CR xenografts; randomized at 250–300 mm³. [4]

Abiraterone delayed the tumor-size endpoint and suppressed tumor androgens. Tumors still progressed; some LuCaP23CR tumors recurred during treatment, whereas LuCaP35CR recurrence occurred after treatment.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Time until tumor-size endpoint (approximately 1000 mm³)	Median endpoint time LuCaP23CR: 14 to 24 days; LuCaP35CR: 17 to 39 days (control to abiraterone).	[4]
Intratumoral testosterone and DHT	Pharmacodynamic response Both suppressed at early sampling (day 7 for LuCaP23CR; days 7–21 for LuCaP35CR).	[4]
Late versus early androgen concentrations in LuCaP35CR	Post-treatment comparison Testosterone increased (p=0.032); DHT increase did not meet p<0.05 (p=0.058).	[4]

Conditions shared by the study groups

Route: Intraperitoneal
Frequency: Daily
Treatment course: 21 days
Vehicle: 5% benzyl alcohol, 95% safflower oil

Study groups and reported outcomes
Group / dose	Comparator	Observed result	Reference
LuCaP23CR abiraterone 0.5 mmol/kg/d	Matched vehicle group	Median time to tumor-size endpoint: 24 days versus 14 days for control; growth 5% per day (95% CI 3.0–6.8%) versus 7.4% (95% CI 6.2–8.0%), p=0.0001.	[4]
LuCaP23CR vehicle	Vehicle control	Comparator values are paired with the abiraterone arm.	[4]
LuCaP35CR abiraterone 0.5 mmol/kg/d	Matched vehicle group	Median time to tumor-size endpoint: 39 days versus 17 days for control; growth 2.5% per day (95% CI 1.2–3.7%) versus 4.8% (95% CI 3.9–5.2%), p<0.0001.	[4]
LuCaP35CR vehicle	Vehicle control	Comparator values are paired with the abiraterone arm.	[4]

LuCaP23CR abiraterone: Model: LuCaP23CR in castrate male CB-17 SCID mice; Reported limits: Model totals: n=46 LuCaP23CR, n=28 LuCaP35CR; exact per-arm endpoint n not stated in reviewed methods.

LuCaP23CR vehicle: Model: LuCaP23CR in castrate male CB-17 SCID mice; Reported limits: Injection volume not stated in reviewed methods.

LuCaP35CR abiraterone: Model: LuCaP35CR in castrate male CB-17 SCID mice; Reported limits: Model totals: n=46 LuCaP23CR, n=28 LuCaP35CR; exact per-arm endpoint n not stated in reviewed methods.

LuCaP35CR vehicle: Model: LuCaP35CR in castrate male CB-17 SCID mice; Reported limits: Injection volume not stated in reviewed methods.

Methods and source locations

Compound reported in the paper: Abiraterone; Compound label in the paper: Abiraterone

Applies to the reported abiraterone experiment; acetate and metabolite results are not assigned to this product.

Methods: LuCaP Human Prostate Cancer Xenografts, Steroid measurements, Statistical Analysis; Results: growth and tumor androgen sections; Figures 2A–D and 3A–D (actual images).

Time until tumor-size endpoint (approximately 1000 mm³): Kaplan–Meier analysis; logrank P = 0.0048 and 0.0014, respectively, in Figure 2. — Methods: LuCaP Human Prostate Cancer Xenografts, Steroid measurements, Statistical Analysis; Results: growth and tumor androgen sections; Figures 2A–D and 3A–D (actual images).

Intratumoral testosterone and DHT: Mass spectrometry; tissue concentrations, not drug exposure. Figure 3 inspected; no plotted values estimated. — Methods: LuCaP Human Prostate Cancer Xenografts, Steroid measurements, Statistical Analysis; Results: growth and tumor androgen sections; Figures 2A–D and 3A–D (actual images).

Late versus early androgen concentrations in LuCaP35CR: Late samples days 29–67 versus early days 7–21; unpaired two-sided t tests in Figure 3. — Methods: LuCaP Human Prostate Cancer Xenografts, Steroid measurements, Statistical Analysis; Results: growth and tumor androgen sections; Figures 2A–D and 3A–D (actual images).

LuCaP23CR abiraterone · Methods: LuCaP Human Prostate Cancer Xenografts, Steroid measurements, Statistical Analysis; Results: growth and tumor androgen sections; Figures 2A–D and 3A–D (actual images).

LuCaP23CR vehicle · Methods: LuCaP Human Prostate Cancer Xenografts, Steroid measurements, Statistical Analysis; Results: growth and tumor androgen sections; Figures 2A–D and 3A–D (actual images).

LuCaP35CR abiraterone · Methods: LuCaP Human Prostate Cancer Xenografts, Steroid measurements, Statistical Analysis; Results: growth and tumor androgen sections; Figures 2A–D and 3A–D (actual images).

LuCaP35CR vehicle · Methods: LuCaP Human Prostate Cancer Xenografts, Steroid measurements, Statistical Analysis; Results: growth and tumor androgen sections; Figures 2A–D and 3A–D (actual images).

LAPC-4 xenograft pharmacodynamic limits

Animal study · Male SCID mice, 4–6 weeks old, bearing bilateral LAPC-4 xenografts; treatment groups formed at average tumor volume at least 90 mm³. [5]

Under this regimen, free abiraterone did not significantly reduce prostate, seminal-vesicle or testis weights and did not significantly change tumor AR protein levels.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Prostate, seminal-vesicle and testis weights	Null pharmacodynamic result No significant reduction versus control.	[5]
Tumor androgen receptor protein	Null pharmacodynamic result No significant effect on AR levels.	[5]

Conditions shared by the study groups

Treatment course: 31 days
Vehicle: 0.3% hydroxypropyl cellulose in 0.9% saline

Study groups and reported outcomes
Group / dose	Comparator	Observed result	Reference
Free abiraterone (3) 0.15 mmol/kg per administration	Vehicle control	No significant organ-weight reduction or AR-protein change.	[5]
Vehicle control	Vehicle control	Reference group for organ weight and AR comparisons.	[5]

Free abiraterone (3): Model: LAPC-4 xenografts in male SCID mice; Route: Subcutaneous; Frequency: Twice daily; Reported limits: 10–12 mice/group stated generally; tumor AR analysis at least 3 tumors/group.

Vehicle control: Model: LAPC-4 xenografts in male SCID mice; Reported limits: Vehicle route/frequency not explicitly specified for this control in the reviewed text.

Methods and source locations

Compound reported in the paper: Abiraterone; Compound label in the paper: 3

Applies to the reported abiraterone experiment; acetate and metabolite results are not assigned to this product.

Figure 1; Methods 2.2.7–2.2.9; Results 3.4 first xenograft study; Figure 6C and Figure 7A–B.

Prostate, seminal-vesicle and testis weights: Organ weights after 31 days; Figure 6C. Exact effect sizes and abiraterone-specific P values not tabulated. — Figure 1; Methods 2.2.7–2.2.9; Results 3.4 first xenograft study; Figure 6C and Figure 7A–B.

Tumor androgen receptor protein: Western blot and densitometry of at least 3 tumors per treatment; Kruskal–Wallis with Dunn post-hoc test; Figure 7. — Figure 1; Methods 2.2.7–2.2.9; Results 3.4 first xenograft study; Figure 6C and Figure 7A–B.

Free abiraterone (3) · Figure 1; Methods 2.2.7–2.2.9; Results 3.4 first xenograft study; Figure 6C and Figure 7A–B.

Vehicle control · Figure 1; Methods 2.2.7–2.2.9; Results 3.4 first xenograft study; Figure 6C and Figure 7A–B.

Specifications

Manufacturer	Adooq Bioscience
Actions	Inhibitor
CAS Number	154229-19-3
Applications	CYP17 inhibitor
Formula	C₂₄H₃₁NO
Molecular Weight	349.2
Synonyms	CB-7598
SMILES	C[C@]12CC[C@@H](CC1=CC[C@@H]3[C@@H]2CC[C@]4([C@H]3CC=C4C5=CN=CC=C5)C)O

Storage & Solubility

In Vitro Solubility

Reported Solubility

No reported solubility data are available for this product.

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

[1] DeVore NM, Scott EE. Structures of cytochrome P450 17A1 with prostate cancer drugs abiraterone and TOK-001. Nature (2012). PMID: 22266943 DOI: 10.1038/nature10743 Source material
[2] Cheong EJY, Nair PC, Neo RWY, et al. Slow-, Tight-Binding Inhibition of CYP17A1 by Abiraterone Redefines Its Kinetic Selectivity and Dosing Regimen. The Journal of pharmacology and experimental therapeutics (2020). PMID: 32554434 DOI: 10.1124/jpet.120.265868 Source material
[3] Petrunak EM, Rogers SA, Aubé J, et al. Structural and Functional Evaluation of Clinically Relevant Inhibitors of Steroidogenic Cytochrome P450 17A1. Drug metabolism and disposition: the biological fate of chemicals (2017). PMID: 28373265 DOI: 10.1124/dmd.117.075317 Source material
[4] Mostaghel EA, Marck BT, Plymate SR, et al. Resistance to CYP17A1 inhibition with abiraterone in castration-resistant prostate cancer: induction of steroidogenesis and androgen receptor splice variants. Clinical cancer research : an official journal of the American Association for Cancer Research (2011). PMID: 21807635 DOI: 10.1158/1078-0432.ccr-11-0728 Source material
[5] Bruno RD, Vasaitis TS, Gediya LK, et al. Synthesis and biological evaluations of putative metabolically stable analogs of VN/124-1 (TOK-001): head to head anti-tumor efficacy evaluation of VN/124-1 (TOK-001) and abiraterone in LAPC-4 human prostate cancer xenograft model. Steroids (2011). PMID: 21729712 DOI: 10.1016/j.steroids.2011.06.002 Source material

Publications

1 publication citing this product

Laurie P. Lee-Glover, .et al. , bioRxiv, 2025, February 17

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Abiraterone (CB-7598)

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Biological Activity

Bioactivity / Mechanism

Target & Activity

Cellular Effect

In Vitro Studies

CYP17A1 binding structure

Literature-Reported Treatment Conditions

Inhibition of CYP17A1 hydroxylase reactions

Literature-Reported Treatment Conditions

Time-dependent CYP17A1 inhibition

Literature-Reported Treatment Conditions

VCaP steroidogenesis and recovery after washout

Literature-Reported Treatment Conditions

In Vivo Studies

LuCaP xenograft growth and intratumoral androgen response

Conditions shared by the study groups

LAPC-4 xenograft pharmacodynamic limits

Conditions shared by the study groups

Specifications

Storage & Solubility

In Vitro Solubility

Reported Solubility

Preparing Stock Solutions

Storage

Research References

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