Cat. No.: HY-18719H

Endoxifen (Z-isomer methanesulfonate)

Endoxifen Z-isomer methanesulfonate is an orally active selective PKCβ1 inhibitor with an IC₅₀ of 360 nM against human PKCβ1. It also acts as an estrogen receptor modulator and antiestrogen. Endoxifen Z-isomer methanesulfonate binds to and blocks ERα, ERβ and PKCβ1, inhibits estrogen and PI3K/AKT/mTORC1 signaling pathways, suppresses the expression of genes associated with cell cycle, cell proliferation and extracellular matrix remodeling, and induces apoptosis, reactive oxygen species (ROS) production and hypoxic features. Endoxifen Z-isomer methanesulfonate inhibits tumor growth in breast tumor and glioblastoma models, reduces bone turnover and blood lipid levels, and does not require metabolism via CYP2D6. It can be used in research related to ER⁺ breast cancer, invasive breast cancer, glioblastoma multiforme, type I bipolar disorder, desmoid tumor, gynecological malignancies, melanoma and hormone receptor-positive solid tumors.

For research use only. We do not sell to patients.

CAS No.: 1032008-71-1
Formula: C₂₆H₃₁NO₅S
Molecular Weight:469.59

Storage:

Please store the product under the recommended conditions in the Certificate of Analysis.

Endoxifen (Z-isomer methanesulfonate) Chemical Structure

CAS No.: 1032008-71-1

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Biological Activity
- Description
- IC₅₀ & Target
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
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References
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Biological Activity

Description

IC₅₀ & Target

^[1]^[2]^[3]^[4]^[5]^[6]^[7]^[8]^[9]^[10]

Human PKCβI

360 nM (IC₅₀)

ERα

ERβ

PI3K

Akt

mTORC1

All PKC Isoforms :

All Estrogen Receptor/ERR Isoforms :

All PI3K Isoforms :

All Akt Isoforms :

All mTOR Isoforms :

In Vitro

Endoxifen Z-isomer (concentrations matching CYP2D6 extensive metabolizers) methanesulfonate is a potent antiestrogen that induces cell-cycle arrest and apoptosis pathways in MCF7 human ER⁺ breast cancer cells, and completely blocks estrogen-stimulated gene expression unlike Tamoxifen (HY-13757A) and its other metabolites^[3].
Endoxifen Z-isomer (0.08-20 μM; 8 days) methanesulfonate potently reduces cell proliferation and induces apoptosis in CRT435 GBM cells, with 20 μM endoxifen alone and in combination with 150 μM TMZ (Temozolomide) (HY-17364) demonstrating significantly greater activity than 250 μM TMZ alone^[4].
Endoxifen Z-isomer (2.5-10 μM; 48 h) methanesulfonate induces significant dose-dependent apoptosis in estrogen-deprived ERα⁺/HER2^- MCF7AC1 breast cancer cells, with the strongest effect observed at 10 μM^[7].
Endoxifen Z-isomer (0.01-5 μM; 72 h) methanesulfonate induces significant apoptosis in estrogen-deprived ERα+/HER2- T47D-LTED breast cancer cells, while lower concentrations (0.01, 0.1 μM) do not^[7].
Endoxifen Z-isomer (5 μM; 24 h) methanesulfonate attenuates AKT^Ser473 phosphorylation and induces PARP cleavage in estrogen-deprived ERα+/HER2- T47D-LTED breast cancer cells^[7].
Endoxifen Z-isomer (5 μM; 48 h incubation, after 48 h cumate pretreatment where applicable) methanesulfonate has its apoptosis-inducing effect significantly diminished by overexpression of constitutively active AKT in estrogen-deprived ERα+/HER2- MCF7AC1caAKT breast cancer cells^[7].
Endoxifen Z-isomer (10 nM-10000 nM; 7 days) methanesulfonate potently inhibits the proliferation of AI-sensitive MCF7AC1 human breast cancer cells in both the presence and absence of Androstenedione^[6].
Endoxifen Z-isomer (10 nM-10000 nM; 7 days) methanesulfonate potently inhibits the proliferation of Letrozole (HY-14248)-resistant MCF7LR human breast cancer cells in both the presence and absence of Androstenedione^[6].
Endoxifen Z-isomer (7 days) methanesulfonate potently inhibits the proliferation of ER+ human breast cancer cells regardless of HER2 status^[6].
Endoxifen Z-isomer (>5 μM; 7 days) methanesulfonate inhibits the proliferation of ER⁻/HER2⁻ MDA-MB-231, MDA-MB-468, and BT20 human breast cancer cells at concentrations greater than 5 μM^[6].
Endoxifen Z-isomer (2.5-10 μM; 48 h) methanesulfonate significantly reduces cell viability in estrogen-deprived ERα+/HER2- MCF7AC1 breast cancer cells, with the strongest effect observed at 10 μM^[7].
Endoxifen Z-isomer (0.01-5 μM; 24 h) methanesulfonate has a minimal impact on the total proteome of estrogen-deprived ERα+/HER2- MCF7AC1 breast cancer cells but induces robust, concentration-dependent changes to the phosphoproteome at 5 μM, with downregulated phosphosites enriched in the PI3K-AKT signaling pathway^[7].
Endoxifen Z-isomer (0.01-5 μM; 24 h) methanesulfonate attenuates AKT^Ser473 phosphorylation and AKT substrate phosphorylation in estrogen-deprived ERα⁺/HER2^- MCF7AC1 breast cancer cells, while lower concentrations (0.01, 0.1 μM) increase AKT^Thr308 phosphorylation without altering AKT^Ser473 or AKT substrate phosphorylation^[7].
Endoxifen Z-isomer (~0.0002-50 μM) methanesulfonate potently inhibits purified PKCβ1 kinase activity in vitro with an IC₅₀ of 360 nM^[7].
Endoxifen Z-isomer (0.01-5 μM; 2 h pretreatment, followed by 20 min 200 nM PMA stimulation) methanesulfonate reduces total PKCβ1 protein levels and attenuates PMA-stimulated AKT^Ser473 phosphorylation and AKT substrate phosphorylation in serum-starved ERα⁺/HER2^- MCF7AC1 breast cancer cells, while lower concentrations (0.01, 0.1 μM) do not elicit these effects^[7].
Endoxifen Z-isomer (100-1000 nM) methanesulfonate inhibits estrogen-induced proliferation in wild-type and ESR1-mutant ER-positive breast cancer cells, with maximum inhibition of ER transcription and estrogen-induced stimulation occurring at concentrations between 100 and 1000 nM, and higher concentrations required for cells with ESR1 mutations or exposed to estradiol concentrations mimicking premenopausal or postmenopausal settings^[9].
Endoxifen Z-isomer (0.1-5 μM; 1 h) methanesulfonate inhibits p-Akt and total Akt protein expression in serum-starved MCF7LR human breast cancer cells after 1 hour of treatment^[6].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Proliferation Assay^[4]

Cell Line:

CRT435 glioblastoma multiforme (GBM) cell line
Concentration:

0.08-20 μM; 20 μM in combination with 150 μM TMZ
Incubation Time:

8 days
Result:

Reduced cell proliferation with a mean difference (Δ) of 269.7 compared to vehicle control, a more pronounced effect than 250 μM TMZ alone (Δ = 142.6).
Reduced cell proliferation with a Δ of 272.8 compared to vehicle control when combined with 150 μM TMZ; both 20 μM endoxifen alone and the combination showed significantly greater inhibition of proliferation than 250 μM TMZ alone (Δ = 127.1 and Δ = 130.2, respectively).
Induced cell death with a Δ of -283181.9 compared to vehicle control, a stronger effect than 250 μM TMZ alone (Δ = -192842.7).
Induced apoptosis with a Δ of -536528.8 compared to vehicle control when combined with 150 μM TMZ, a significantly greater effect than 250 μM TMZ alone (Δ = 343686.2) and comparable to the positive control (10% DMSO, Δ = -581979.3).

Cell Proliferation Assay^[6]

Cell Line:

Aromatase-expressing MCF7AC1 (AI-sensitive) human breast cancer cells
Concentration:

10 nM-10000 nM (presence of androstenedione); 10 nM-10000 nM (absence of androstenedione)
Incubation Time:

7 days (presence of androstenedione); 7 days (absence of androstenedione)
Result:

Potently inhibited MCF7AC1 cell growth, with activity superior to tamoxifen and similar to fulvestrant.
Reduced cell growth to near 0% of control at 10000 nM in the presence of androstenedione.
Reduced cell growth to near 0% of control at 10000 nM in the absence of androstenedione.

Cell Proliferation Assay^[6]

Cell Line:

Letrozole-resistant MCF7LR human breast cancer cells
Concentration:

10 nM-10000 nM (presence of androstenedione); 10 nM-10000 nM (absence of androstenedione)
Incubation Time:

7 days (presence of androstenedione); 7 days (absence of androstenedione)
Result:

Potently inhibited MCF7LR cell growth, with activity superior to tamoxifen and similar to fulvestrant.
Reduced cell growth to near 0% of control at 10000 nM in the presence of androstenedione.
Reduced cell growth to near 0% of control at 10000 nM in the absence of androstenedione.

Cell Proliferation Assay^[6]

Cell Line:

ER−/HER2− human breast cancer cells (MDA-MB-231, MDA-MB-468, BT20)
Concentration:

>5 μM (presence of estrogen); >5 μM (absence of estrogen)
Incubation Time:

7 days (presence of estrogen); 7 days (absence of estrogen)
Result:

Exhibited antiproliferative activity at concentrations >5 μM, with a pattern of activity similar to tamoxifen and 4-hydroxytamoxifen, both in the presence and absence of estrogen.

Western Blot Analysis^[6]

Cell Line:

Serum-starved MCF7LR human breast cancer cells
Concentration:

0.1 μM; 5 μM
Incubation Time:

1 h
Result:

Effectively inhibited both p-Akt and total Akt protein levels relative to ethanol control at 5 μM.
Did not induce p-Akt levels, unlike letrozole, tamoxifen, and 4-hydroxytamoxifen treatments.

Cell Viability Assay^[7]

Cell Line:

Estrogen-deprived ERα+/HER2- MCF7AC1 breast cancer cells
Concentration:

0.01-10 μM
Incubation Time:

48 h
Result:

Reduced cell viability to ~55% of control at 10 μM.
Reduced cell viability to ~75% of control at 7.5 μM.
Reduced cell viability to ~85% of control at 5 μM.
Did not significantly affect cell viability at concentrations below 2.5 μM.

Apoptosis Analysis^[7]

Cell Line:

Estrogen-deprived ERα+/HER2- MCF7AC1 breast cancer cells
Concentration:

0.01-10 μM
Incubation Time:

48 h
Result:

Induced ~80% apoptosis at 10 μM.
Induced ~75% apoptosis at 7.5 μM.
Induced ~50% apoptosis at 5 μM.
Did not significantly induce apoptosis at concentrations below 2.5 μM.

Western Blot Analysis^[7]

Cell Line:

Estrogen-deprived ERα+/HER2- MCF7AC1 breast cancer cells
Concentration:

0.01 μM; 0.1 μM; 5 μM
Incubation Time:

24 h
Result:

Reduced pAKTSer473 levels to 50% of control at 5 μM, with no significant effect at 0.01 μM and 0.1 μM.
Increased pAKTThr308 levels to 221% of control at 0.01 μM and 0.1 μM, with no significant effect at 5 μM.
Reduced phosphorylation of AKT substrates only at 5 μM.

Western Blot Analysis^[7]

Cell Line:

serum-starved ERα+/HER2- MCF7AC1 breast cancer cells
Concentration:

0.01 μM; 0.1 μM; 5 μM
Incubation Time:

2 h pretreatment, followed by 1 h 100 nM insulin stimulation
Result:

Blocked insulin-stimulated pAKTSer473 and pAKTThr308 phosphorylation at 5 μM, with no effect at 0.01 μM and 0.1 μM.
Diminished insulin-stimulated phosphorylation of AKT substrates at 5 μM, with no effect at lower concentrations.

Western Blot Analysis^[7]

Cell Line:

serum-starved ERα+/HER2- MCF7AC1 breast cancer cells
Concentration:

0.01-5 μM
Incubation Time:

2 h pretreatment, followed by 20 min 200 nM PMA stimulation
Result:

Reduced total PKCβ1 levels to 29% of control at 5 μM, with no significant effect at 0.01 μM and 0.1 μM.
Attenuated PMA-stimulated pAKTSer473 phosphorylation and AKT substrate phosphorylation at 5 μM, with no effect at lower concentrations.
Had minimal to no effect on PMA-stimulated pPKCβ1Ser661 phosphorylation at all tested concentrations.

Apoptosis Analysis^[7]

Cell Line:

estrogen-deprived ERα+/HER2- T47D-LTED breast cancer cells
Concentration:

0.01-5 μM
Incubation Time:

72 h
Result:

Induced significant apoptosis reaching ~50% at 5 μM.
Did not significantly induce apoptosis at 0.01 μM and 0.1 μM.

Western Blot Analysis^[7]

Cell Line:

estrogen-deprived ERα+/HER2- T47D-LTED breast cancer cells
Concentration:

0.01-5 μM
Incubation Time:

24 h
Result:

Reduced pAKTSer473 levels to 61% of control at 5 μM, with no significant effect at 0.01 μM and 0.1 μM.
Increased cleaved PARP levels to 1.58-fold of control at 5 μM, with no significant effect at lower concentrations.

Apoptosis Analysis^[7]

Cell Line:

estrogen-deprived ERα+/HER2- MCF7AC1caAKT breast cancer cells (with cumate-induced constitutively active AKT expression)
Concentration:

5 μM
Incubation Time:

48 h incubation, after 48 h cumate pretreatment where applicable
Result:

Induced significant apoptosis reaching ~90% by 48 hours in the absence of cumate.
Induced significantly less apoptosis reaching ~45% by 48 hours with no significant difference vs control in the presence of cumate (active AKT overexpression).

Parmacokinetics

Species	Dose	Route	Plasma Concentration
Mice^[6]	25 mg/kg	p.o.	11.8 ng/mL
Mice^[6]	75 mg/kg	p.o.	391.3 ng/mL

In Vivo

Endoxifen (Z-isomer methanesulfonate) (5 mg/kg; s.c.; daily; via extended-release pellet replaced every 90 days) significantly increases tumor latency to 111 days, reduces tumor burden by 76%, and reduces tumor multiplicity by 63% in a tamoxifen-insensitive spontaneous aggressive breast cancer mouse model, while downregulating key pathways related to cell proliferation, tumor remodeling, and immune modulation^[2].
Endoxifen Z-isomer (5 mg/kg; s.c.; daily; via extended-release pellet replaced every 90 days) methanesulfonate combined with Ulipristal acetate (HY-16508) (16.7 mg/kg/day; s.c.; daily; via extended-release pellet replaced every 30 days) shows no improvement in breast cancer preventive efficacy compared to endoxifen monotherapy; this combination fails to significantly prolong tumor latency, decrease tumor burden, or suppress the expression of critical poor-prognosis genes^[2].
Endoxifen Z-isomer (50 mg/kg; p.o.; daily; 4 weeks) methanesulfonate demonstrates superior antitumor activity against Letrozole-resistant ER+ breast cancer xenografts, with potent suppression of proliferation marker Ki-67, ERα target genes, and Akt signaling^[6].
Endoxifen Z-isomer (25-75 mg/kg; p.o.; daily; 28 days) methanesulfonate, administered as monotherapy or in combination with TMZ, does not significantly reduce tumor volume in a subcutaneous CRT435 GBM PDX athymic nude mouse model, despite being well tolerated^[4].
Endoxifen Z-isomer (25-75 mg/kg; p.o.; daily; 4 weeks) methanesulfonate exhibits superior antitumor activity against AI-sensitive ER⁺ breast cancer xenografts, with the 75 mg/kg dose also outperforming letrozole^[6].
Endoxifen Z-isomer (50 mg/kg; p.o.; 5 days a week) methanesulfonate exhibits potent, prolonged antitumor activity against Letrozole-resistant ER⁺ breast cancer xenografts^[6].
Endoxifen Z-isomer (10-50 mg/kg) methanesulfonate at 10 mg/kg and 50 mg/kg exerts beneficial skeletal effects and modulates uterine gene expression in intact and ovariectomized Sprague-Dawley rats^[7].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

C3(1)-TAg (FVB/NJ × FVB/C3(1)-TAg) (female, 8 weeks old)^[2]
Dosage:

5 mg/kg
Administration:

s.c.; daily; via extended-release pellet replaced every 90 days
Result:

Produced a tumor penetrance of 92% (11/12 mice) with a significant increase in tumor latency to 111 days compared to untreated controls.
Reduced median tumor burden by 76% to 0.273 cm³ and reduced median tumor multiplicity by 63% to 3 tumors per animal compared to controls.
Reduced mammary intraepithelial neoplasia (MIN) multiplicity in tumor-bearing glands by 43% to 4 lesions per gland, and had the highest proportion of mice with at least one tumor-free gland (92%, 11/12 mice).
Induced a nonsignificant 17% decline in pHH3 labeling index (cell proliferation marker) in MIN lesions (7.2 vs. 8.7) and 23% decrease in benign tissue (7 vs. 9.1) compared to controls.
Significantly downregulated 39% (43/111) of a panel of target genes, including 24 genes unique to endoxifen therapy; these genes mapped to downregulated biological pathways including cell cycle, oocyte meiosis, E2F transcription factor network, cytokine-cytokine receptor interaction, EGF/EGFR signaling pathway, and integrated breast cancer pathway.
Also significantly downregulated genes associated with poor breast cancer prognosis (Col11a1, Il17b, Pdgfa, Tnfrsf11a).
Median plasma endoxifen concentration was 8.7 ng/mL (22.4 nM).

Animal Model:

C3(1)-TAg (FVB/NJ × FVB/C3(1)-TAg) (female, 8 weeks old)^[2]
Dosage:

5 mg/kg/day endoxifen + 16.7 mg/kg/day ulipristal acetate
Administration:

s.c.; daily; endoxifen via extended-release pellet replaced every 90 days, ulipristal acetate via extended-release pellet replaced every 30 days
Result:

Produced a tumor penetrance of 88% (7/8 mice) with a nonsignificant increase in tumor latency to 108 days and nonsignificant 59% reduction in median tumor burden to 0.45 cm³ compared to controls.
Did not significantly affect tumor multiplicity (9 vs. 8 tumors per animal) or MIN multiplicity in tumor-bearing glands (6 vs. 7 lesions per gland).
Induced a reduction in pHH3 labeling index in tumor-free glands, which was significantly less effective than endoxifen monotherapy.
Modulated 32% (36/111) of a panel of target genes, with 75% overlap with endoxifen-modulated genes; unlike endoxifen monotherapy, it did not repress several genes associated with poor prognosis (Dbc1, Il17b, Il24, Pdgfa, Serpina5, Tnfrsf11a).
Median plasma endoxifen concentration was 12 ng/mL (31.3 nM), significantly higher than in mice treated with tamoxifen alone.

Animal Model:

athymic nude mice (female, 6-12 weeks old, average weight ~26 g, implanted subcutaneously with CRT435 patient-derived xenograft tumor)^[4]
Dosage:

25 mg/kg; 50 mg/kg; 75 mg/kg
Administration:

p.o.; daily; 28 days
Result:

Did not produce significant tumor growth reduction compared to vehicle control group.
Did not produce significant tumor regression when combined with intratumoral TMZ compared to vehicle control group.
Showed no significant impact on mouse body weight over the 28-day study period.

Animal Model:

BALB/c athymic nude mice (4-6-week-old, ovariectomized female, subcutaneous xenograft of MCF7AC1 aromatase-expressing ER+ breast cancer cells, supplemented with 1.4-mg 90-day-release estrogen pellets)^[6]
Dosage:

25 mg/kg; 75 mg/kg
Administration:

p.o.; daily; 4 weeks
Result:

Significantly reduced tumor volumes compared to control and tamoxifen at 4 weeks.
Yielded plasma concentrations of 11.8 ng/mL (25 mg/kg) and 391.3 ng/mL (75 mg/kg) at 2 weeks.
Significantly reduced murine body weight at 4 weeks (75 mg/kg dose).
Was superior to letrozole at 75 mg/kg dose.

Animal Model:

Athymic nude mice (ovariectomized female, subcutaneous xenograft of letrozole-resistant MCF7LR ER+ breast cancer cells derived from MCF7AC1 tumors)^[6]
Dosage:

50 mg/kg
Administration:

p.o.; daily; 4 weeks
Result:

Significantly reduced tumor volume compared to tamoxifen.
Significantly suppressed nuclear Ki-67 expression compared to letrozole-treated MCF7LR tumors.
Downregulated ERα target genes AREG (-3.2 fold), PGR (-4.8 fold, p = 4.34×10^-8), and TFF1 (-6.8 fold).
Reduced p-Akt protein levels in tumor tissue.

Animal Model:

Athymic nude mice (6-7-week-old, ovariectomized female, subcutaneous xenograft of MCF7LR ER+ breast cancer cells, supplemented with 100 μg/day androstenedione 5 days a week)^[6]
Dosage:

50 mg/kg
Administration:

p.o.; 5 days a week
Result:

Potently inhibited tumor growth over 9 weeks (63 days), with antitumor activity superior to letrozole and exemestane (p = 0.03), and not significantly different from exemestane plus everolimus or fulvestrant.
Reduced mean tumor volume compared to letrozole, which failed to inhibit growth, and delayed tumor growth beyond the 23-week time point seen with exemestane plus everolimus.
Significantly reduced body weight, which was mitigated by oral nutritional supplement.

Chemical Information

CAS No. 1032008-71-1
Molecular Weight 469.59
Formula C₂₆H₃₁NO₅S
SMILES

CS(=O)(O)=O.CC/C(C1=CC=CC=C1)=C(C2=CC=C(C=C2)O)/C3=CC=C(C=C3)OCCNC
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation

Handling Instructions (2659 KB)

References

[1]. Elkins P, et al. Characterization of the isomeric configuration and impurities of (Z)-endoxifen by 2D NMR, high resolution LC⬜MS, and quantitative HPLC analysis. Journal of pharmaceutical and biomedical analysis. 2014 Jan;88:174-9. [Content Brief]

[2]. Lee O, et al. Z-Endoxifen prevents aggressive mammary cancers in mice by inhibiting cell proliferation and creating a tumor suppressive microenvironment. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. 2023 Jun;162:114607. [Content Brief]

[3]. Jayaraman S, et al. Endoxifen, an Estrogen Receptor Targeted Therapy: From Bench to Bedside. Endocrinology. 2021 Dec 01;162(12):bqab191. [Content Brief]

[4]. Shneyderman A, et al. Evaluation of (Z)-endoxifen as a potential therapy for glioblastoma multiforme through computational and experimental analyses. Scientific reports. 2025 Oct 31;15(1):38225. [Content Brief]

[5]. Nardin JM, et al. The Influences of Adherence to Tamoxifen and CYP2D6 Pharmacogenetics on Plasma Concentrations of the Active Metabolite (Z)-Endoxifen in Breast Cancer. Clinical and translational science. 2020 Mar;13(2):284-292. [Content Brief]

[6]. Jayaraman S, et al. Antitumor activity of Z-endoxifen in aromatase inhibitor-sensitive and aromatase inhibitor-resistant estrogen receptor-positive breast cancer. Breast cancer research : BCR. 2020 May 19;22(1):51. [Content Brief]

[7]. Jayaraman S, et al. Endoxifen downregulates AKT phosphorylation through protein kinase C beta 1 inhibition in ERα+ breast cancer. NPJ breast cancer. 2023 Dec 19;9(1):101. [Content Brief]

[8]. Sanchez-Spitman AB, et al. Clinical pharmacokinetics and pharmacogenetics of tamoxifen and endoxifen. Expert review of clinical pharmacology. 2019 Jun;12(6):523-536. [Content Brief]

[9]. Goetz MP, et al. First-in-Human Phase I Study of the Tamoxifen Metabolite Z-Endoxifen in Women With Endocrine-Refractory Metastatic Breast Cancer. Journal of clinical oncology : official journal of the American Society of Clinical Oncology. 2017 Oct 20;35(30):3391-3400. [Content Brief]

[10]. Takebe N, et al. Phase 1 study of Z-endoxifen in patients with advanced gynecologic, desmoid, and hormone receptor-positive solid tumors. Oncotarget. 2021 Feb 16;12(4):268-277. [Content Brief]

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Endoxifen (Z-isomer methanesulfonate)

All PKC Isoforms

All Estrogen Receptor/ERR Isoforms

All PI3K Isoforms

All Akt Isoforms

All mTOR Isoforms