Ro 48-8071 fumarate targets 2,3-oxidosqualene:lanosterol cyclase (OSC, E.C. 5.4.99.7, also named lanosterol synthase/intramolecular transferases) [1]
Ro 48-8071 fumarate exerts anti-cancer effects via modulating estrogen receptor α (ERα) and estrogen receptor β (ERβ) expression in breast cancer cells, and androgen receptor (AR) expression in prostate cancer cells; [2]
Ro 48-8071 fumarate modulates ERα/ERβ expression in hormone-dependent breast cancer cells, [3]
Ro 48-8071 fumarate selectively inhibits intestinal OSC activity to suppress cholesterol synthesis [4]

With an IC50 value of roughly 1.5 nM, Ro 48 -8071 decreases cholesterol synthesis in HepG2 cells in a dose-dependent manner [1]. The viability of PC-3 prostate cancer cells is significantly reduced by Ro 48 -8071 (10 μM), but not of normal prostate cells. In LNCaP and C4-2 cell lines, Ro 48 -8071 (10-30 μM) causes apoptosis in a dose-dependent manner. Significant levels of apoptosis were also seen in castration-resistant PC-3 and DU145 cells 24 hours after they were treated with Ro 48–8071. The reduction of AR protein expression is dose-dependent and occurs with Ro 48 -8071 (10-25 μM). In castration-resistant PC-3 cells and hormone-dependent LNCaP, Ro 48 -8071 (0.1-1 μM) dose-dependently upregulates the expression of the ERβ protein [2]. Mammalian cells engineered to express human ERα or ERβ proteins in combination with the ER-responsive luciferase promoter, enables Ro 48-8071 to dose-dependently inhibit 17β-estradiol (E2)-induced ERα-responsive luciferase. Activity (IC50, approximately 10 μM), in a cell-nontoxic environment [3].

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1. Ro 48-8071 fumarate blocked human liver OSC activity and cholesterol synthesis in HepG2 cells in the nanomolar range; it triggered the production of monooxidosqualene, dioxidosqualene, and epoxycholesterol in HepG2 cells [1]
2. Ro 48-8071 fumarate reduced viability of hormone-dependent (LNCaP) and castration-resistant (PC-3, DU145) prostate cancer cell lines in a concentration-dependent manner (evaluated by SRB assay): LNCaP cells (7×10³/well) in 20% FBS RPMI-1640 were treated with RO in 10% FBS RPMI-1640 for 24/48 h; PC-3/DU145 cells (4×10³/well) in 10% FBS RPMI-1640 were treated with RO in 5% FBS RPMI-1640 for 24/48 h, with significant reduction in cell viability (P<0.05); RO had no effect on viability of normal human prostate RWPE-1 cells (5×10³/well) in complete growth medium treated with RO for 24 h (SRB assay, P>0.05) [2]
3. Low-dose (nM range) Ro 48-8071 fumarate treatment for 7 days reduced viability of LNCaP (8×10⁴/well, 10% FBS RPMI-1640) and PC-3 (4×10⁴/well, 5% FBS RPMI-1640) prostate cancer cells (SRB assay, P<0.05), with RO retreated every 48 h [2]
4. Ro 48-8071 fumarate induced apoptosis in hormone-dependent (LNCaP, C4-2) and castration-resistant (PC-3, DU145) prostate cancer cells: LNCaP (4×10⁵/well, 20% FBS RPMI-1640) and C4-2 (3×10⁵/well, 10% FBS RPMI-1640) cells were treated with RO (μM range) in 10%/5% FBS RPMI-1640 for 24 h; PC-3/DU145 (3×10⁵/well, 10% FBS RPMI-1640) cells were treated with RO (μM range) for 24 h; apoptotic/dead cells were quantified by Annexin V-FITC–based FACS analysis (P<0.05) [2]
5. Ro 48-8071 fumarate reduced AR protein expression in LNCaP prostate cancer cells (70% confluency, 20% FBS RPMI-1640) treated with 10/25 μM RO for 6 h or 0.1–1.0 μM RO for 7 days (Western blot); it increased ERβ protein expression in LNCaP (20% FBS RPMI-1640) and PC-3 (10% FBS RPMI-1640) cells treated with 10/25 μM RO for 6 h (Western blot) [2]
6. Combining Ro 48-8071 fumarate (15 μM, 2 h pretreatment + 22 h treatment) with ERβ agonist DPN (100 nM, 22 h treatment) potentiated the reduction of PC-3 cell viability (SRB assay, P<0.001); DPN alone (100 nM, 22 h) also reduced PC-3 viability (P=0.041) [2]
7. Ro 48-8071 fumarate potently reduced viability of ER-positive human breast cancer cells (BT-474, MCF-7, T47-D) in a concentration-dependent manner (pharmacological doses, 48 h treatment, SRB assay, P<0.05); low-dose (nM range) RO treatment for 7 days also reduced breast cancer cell viability (SRB assay, P<0.05); RO had no effect on viability of normal human mammary cells (AG11132A) treated with pharmacological doses for 24 h (SRB assay, P>0.05) [3]
8. Ro 48-8071 fumarate induced apoptosis and cell death in BT-474 and MCF-7 breast cancer cells: cells (1.5×10⁵/well, 10% FBS DMEM:F12) were treated with 5/10/20 μM RO for 24 h; apoptotic (Annexin V-positive) and dead (Annexin V-positive/PI-positive) cells were quantified by FACS analysis (10,000 cells/sample, P<0.05) [3]
9. Ro 48-8071 fumarate suppressed Estradiol (E2)-induced proliferation of breast cancer cells: cells were treated with 10 nM E2 ± 1/5/10 μM RO or 1 μM ICI 182,780 for 24 h in 5% charcoal stripped serum (SRB assay, P<0.05 vs E2 alone) [3]
10. Ro 48-8071 fumarate degraded ERα and induced ERβ expression in breast cancer cells: BT-474/MCF-7/T47-D cells (5% FBS DMEM:F12) were treated with 1/5/10/25 μM RO for 3/6/12 h (Western blot); ERβ inhibition/knockdown prevented RO-dependent loss of breast cancer cell viability (SRB assay, P<0.001) [3]
11. Combining Ro 48-8071 fumarate (10 μM, 48 h) with ERβ agonist DPN (1 μM) potentiated reduction of BT-474 cell viability (SRB assay, P<0.001); combining RO (10 μM, 24 h) with ERβ antagonist PHTPP (10/100 nM) reversed RO-induced loss of BT-474 viability (SRB assay, P<0.001) [3]

In hamsters, Ro 48 -8071 decreases LDL-C by approximately 60% at 150 μmol/kg per day and stops at 300 μmol/kg per day; HDL-C does not change at any dose. The amount of MOS in hamster liver increases at Ro 48 -8071 (≥00 μMol/kg per day). In hamsters, Ro 48 -8071 (300 μmol/kg daily) dramatically lowers VLDL secretion [1]. Without causing weight loss, Ro 48 -8071 (5 or 20 mg/kg) dramatically slowed the growth of tumors in mice. Furthermore, two of the twelve tumors observed in mice during the test period were totally eradicated by Ro 48-8071 at a dosage of 20 mg/kg [2]. In the entire small intestine of BALB/c mice, Ro 48-8071 (20 mg/day/kg body weight) rapidly and persistently inhibits (>50%) the synthesis of cholesterol. Additionally, the stomach and large intestine produce less cholesterol [4].

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1. Ro 48-8071 fumarate was safe at pharmacologically active doses in hamsters, squirrel monkeys, and Göttingen minipigs; it lowered LDL cholesterol by approximately 60% in hamsters, and at least 30% in squirrel monkeys and minipigs, with efficacy comparable to safe doses of simvastatin; hepatic monooxidosqualene increased dose-dependently after RO treatment (up to ~20 μg/g wet liver, <1% of hepatic cholesterol) and was inversely correlated with LDL levels [1]
2. Ro 48-8071 fumarate did not reduce coenzyme Q10 levels in liver and heart of hamsters, and did not trigger overexpression of hepatic HMG-CoA reductase, squalene synthase, or OSC; in contrast, simvastatin stimulated these enzymes and reduced coenzyme Q10 levels in liver and heart [1]
3. Ro 48-8071 fumarate effectively suppressed growth of aggressive castration-resistant PC-3 prostate cancer cell xenografts in male athymic nu/nu nude mice: PC-3 cells (5×10⁶ in 0.15 mL, matrigel:RPMI-1640=1:1 v/v) were injected subcutaneously into both flanks of 6-week-old mice; when tumors reached ~100 mm³, RO was administered by tail vein injection (5/20 mg/kg/d for 5 days as loading dose, then same dose every other day for 6 additional treatments, final injection 2 h before sacrifice); tumor volume was significantly reduced (P<0.05), with 2 out of 12 tumors in the 20 mg/kg group completely eradicated; no significant changes in animal weight were observed [2]
4. Ro 48-8071 fumarate prevented growth of BT-474 breast cancer xenografts in nude mice: 6-week-old nude mice received 1.7 mg/60-days estradiol slow-release pellets sc 48 h prior to injection of BT-474 cells (5×10⁶, Matrigel:DMEM/F12=4:1 v/v) into both flanks; when tumors reached ~100 mm³, RO was administered iv (5/10 mg/kg/d for 5 days, then every other day for 5 additional treatments, final injection 2 h before sacrifice); tumor growth was significantly inhibited (P<0.05), with no apparent toxicity (no weight loss); RO reduced ERα and increased ERβ staining in tumor tissues (immunohistochemistry, P<0.05) [3]
5. Ro 48-8071 fumarate (20 mg/day/kg bw, fed in chow diet for 7 days) induced rapid and sustained inhibition (>50%) of cholesterol synthesis in the whole small intestine of BALB/c mice; sterol synthesis was also reduced in the large intestine and stomach; hepatic cholesterol synthesis was markedly suppressed initially but rebounded to above baseline within 7 days; whole body cholesterol synthesis, fractional cholesterol absorption, and fecal neutral/acidic sterol excretion were not consistently changed [4]
6. Ro 48-8071 fumarate (20 mg/day/kg bw, 7 days) reduced sterol synthesis in liver, small intestine, large intestine, stomach of female BALB/c mice (measured by [³H] water incorporation into sterols); no significant changes in whole animal sterol synthesis (10 days treatment) were observed [4]
7. Ro 48-8071 fumarate (20 mg/day/kg bw, 10 days) reduced intestinal cholesterol synthesis in LDLR-deficient (ldlr−/−) mice and wild-type (ldlr+/+) controls (129/Sv background), with no significant genotype-dependent differences in intestinal/hepatic cholesterol concentration or sterol synthesis [4]
8. Ro 48-8071 fumarate (20 mg/day/kg bw, 18 days) had no significant effect on hepatic/plasma cholesterol concentrations in BALB/c mice fed a high cholesterol diet (1.0% w/w cholesterol); it did not alter mRNA levels of bile acid synthesis-related genes in liver [4]

1. OSC activity assay (human liver/ HepG2 cells): Cells/liver homogenates were incubated with OSC substrates (2,3-oxidosqualene) in the presence/absence of Ro 48-8071 fumarate (nanomolar range); cholesterol synthesis was measured by quantifying cholesterol production, and OSC activity was assessed by measuring lanosterol synthesis; the production of monooxidosqualene, dioxidosqualene, and epoxycholesterol was quantified to evaluate the downstream effects of OSC inhibition [1]
2. Cholesterol synthesis assay (HepG2 cells): HepG2 cells were treated with Ro 48-8071 fumarate (nanomolar range); intracellular cholesterol levels were quantified, and the production of oxidosqualene metabolites (monooxidosqualene, dioxidosqualene, epoxycholesterol) was measured via chromatographic methods to confirm OSC inhibition [1]
3. Sterol synthesis assay (mouse/hamster tissues): Tissue homogenates (small intestine, liver, large intestine, stomach) from animals treated with Ro 48-8071 fumarate were incubated with [³H] water; the incorporation of [³H] water into sterols was measured (nmol/h/g tissue) to assess de novo cholesterol synthesis and OSC activity; whole animal sterol synthesis was measured as umol of [³H] water incorporated into sterols/h/100 g bw [4]

1. Prostate cancer cell viability assay: LNCaP (7×10³/well) were seeded in 96-well plates with 20% FBS RPMI-1640 overnight; PC-3/DU145 (4×10³/well) were seeded with 10% FBS RPMI-1640 overnight; cells were washed with FBS-free medium, then treated with varying concentrations of Ro 48-8071 fumarate in 10% FBS RPMI-1640 (LNCaP) or 5% FBS RPMI-1640 (PC-3/DU145) for 24/48 h; cell viability was evaluated by SRB assay, with absorbance measured to quantify cell proliferation [2]
2. Normal prostate cell viability assay: RWPE-1 cells (5×10³/well) were seeded in 96-well plates with complete growth medium overnight; PC-3 cells (4×10⁴/well) were seeded with 10% FBS RPMI-1640 overnight; cells were washed with FBS-free medium, then treated with varying concentrations of Ro 48-8071 fumarate in complete growth medium (RWPE-1) or 5% FBS RPMI-1640 (PC-3) for 24 h; cell viability was assessed by SRB assay [2]
3. Long-term prostate cancer cell viability assay: LNCaP (8×10⁴/well) were seeded in 6-well plates with 20% FBS RPMI-1640 overnight; PC-3 (4×10⁴/well) were seeded with 10% FBS RPMI-1640 overnight; cells were washed with FBS-free medium, then treated with low-dose (nM) Ro 48-8071 fumarate in 10% FBS RPMI-1640 (LNCaP) or 5% FBS RPMI-1640 (PC-3) for 7 days (RO retreated every 48 h); cell viability was measured by SRB assay [2]
4. Prostate cancer cell apoptosis assay: LNCaP (4×10⁵/well) were seeded in 6-well plates with 20% FBS RPMI-1640 overnight; C4-2 (3×10⁵/well) were seeded with 10% FBS RPMI-1640 overnight; PC-3/DU145 (3×10⁵/well) were seeded with 10% FBS RPMI-1640 overnight; cells were washed with FBS-free medium, then treated with μM concentrations of Ro 48-8071 fumarate for 24 h; cells were harvested, stained with Annexin V-FITC and PI, and apoptotic/dead cells were quantified by FACS analysis (10,000 cells per sample) [2]
5. AR/ERβ expression assay (prostate cancer cells): LNCaP cells (70% confluency, 20% FBS RPMI-1640) were treated with 10/25 μM Ro 48-8071 fumarate for 6 h or 0.1–1.0 μM RO for 7 days; PC-3 cells (70% confluency, 10% FBS RPMI-1640) were treated with 10/25 μM RO for 6 h; whole-cell extracts were prepared, and AR/ERβ protein expression was analyzed by Western blotting with specific antibodies (β-actin as loading control) [2]
6. Breast cancer cell viability assay: BT-474/MCF-7/T47-D breast cancer cells were seeded in 96-well plates and treated with pharmacological/nM concentrations of Ro 48-8071 fumarate for 24/48/7 days (media change every 48 h for 7-day treatment); normal mammary cells (AG11132A) were treated with pharmacological doses of RO for 24 h; cell viability was evaluated by SRB assay, with absorbance measured to quantify cell proliferation [3]
7. Breast cancer cell apoptosis assay: BT-474/MCF-7 cells (1.5×10⁵/well) were seeded in 6-well plates with 10% FBS DMEM:F12 overnight; cells were washed with FBS-free medium, treated with 5/10/20 μM Ro 48-8071 fumarate for 24 h, harvested, stained with Annexin V-FITC and PI, and apoptotic/dead cells were quantified by FACS analysis (10,000 cells per sample) [3]
8. ERα/ERβ expression assay (breast cancer cells): BT-474/MCF-7/T47-D cells (70% confluency, 5% FBS DMEM:F12) were treated with 1/5/10/25 μM Ro 48-8071 fumarate for 3/6/12 h; whole-cell extracts were prepared, and ERα/ERβ protein expression was analyzed by Western blotting (β-actin as loading control); for ERβ knockdown assay, T47-D cells were transfected with 30/60 nM ERβ siRNA or scrambled siRNA for 72 h, then treated with 10 μM RO for 48 h, and cell viability was measured by SRB assay [3]
9. E2-induced breast cancer cell proliferation assay: Breast cancer cells were seeded in 96-well plates with 5% charcoal stripped serum, treated with 10 nM E2 ± 1/5/10 μM Ro 48-8071 fumarate or 1 μM ICI 182,780 for 24 h; cell viability was evaluated by SRB assay to assess the suppression of E2-induced proliferation [3]

150, 300 μmol/kg
BALB/c mice

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1. Hamster/squirrel monkey/minipig cholesterol-lowering assay: Ro 48-8071 fumarate was administered to hamsters, squirrel monkeys, and Göttingen minipigs at pharmacologically active doses (dose not specified); simvastatin was administered as a control (doses >30 μmol/kg/day caused hepatotoxicity in hamsters); plasma LDL cholesterol levels were measured at regular intervals; hepatic monooxidosqualene levels and coenzyme Q10 levels (liver/heart) were quantified; hepatic gene expression (HMG-CoA reductase, squalene synthase, OSC) was analyzed [1]
2. Prostate cancer xenograft assay (nude mice): 6-week-old male athymic nu/nu nude mice were used; PC-3 cells (5×10⁶) were mixed with matrigel and RPMI-1640 (1:1 v/v) to a final volume of 0.15 mL, then injected subcutaneously into both flanks; when tumor volume reached ~100 mm³, Ro 48-8071 fumarate was administered by tail vein injection: 5/20 mg/kg/day for 5 days (loading dose), followed by the same dose every other day for 6 additional treatments, with a final injection 2 h before sacrifice; control mice received vehicle alone; tumor volume and animal weight were monitored throughout the experiment; tumors were harvested and photographed at the end [2]
3. Breast cancer xenograft assay (nude mice): 6-week-old nude mice received a 1.7 mg/60-days estradiol slow-release pellet via subcutaneous implantation 48 h before tumor cell injection; BT-474 cells (5×10⁶) were mixed with Matrigel and DMEM/F12 (4:1 v/v), then injected subcutaneously into both flanks; when tumor volume reached ~100 mm³, Ro 48-8071 fumarate was administered via tail vein injection: 5/10 mg/kg/day for 5 days, then every other day for 5 additional treatments, with a final injection 2 h before sacrifice; control mice received PBS alone; tumor volume and animal weight were monitored; tumors were harvested for immunohistochemistry (ERα/ERβ staining) [3]
4. Mouse intestinal cholesterol synthesis assay (BALB/c mice): Female/male BALB/c mice (7–16 weeks old) were fed a rodent chow diet containing Ro 48-8071 fumarate at doses of 5/15/20 mg/day/kg bw for 12 h to 18 days; simvastatin (20/200 mg/day/kg bw) was used as a control for 0.5–7 days; sterol synthesis rates in small intestine, liver, large intestine, stomach, and other organs were measured via [³H] water incorporation assay; intestinal histology (H&E staining) and Ki67 immunochemistry were performed; mRNA expression of intestinal cholesterol regulation genes (NPC1L1, CYP3A11, CES2A) was analyzed [4]
5. LDLR-deficient mouse assay (ldlr−/− mice): Female ldlr−/− mice and ldlr+/+ controls (21–25 weeks old, 129/Sv background) were fed a rodent chow diet containing Ro 48-8071 fumarate (20 mg/day/kg bw) for 10 days; intestinal/hepatic cholesterol concentration and sterol synthesis rates were measured; plasma cholesterol levels were quantified [4]
6. High cholesterol diet mouse assay: Female BALB/c mice (10–16 weeks old) were fed a rodent chow diet (0.02% w/w inherent cholesterol) supplemented with 1.0% w/w cholesterol, with/without Ro 48-8071 fumarate (20 mg/day/kg bw) for 18 days; hepatic/plasma cholesterol concentrations and mRNA levels of bile acid synthesis genes were measured; fecal neutral/acidic sterol excretion was quantified [4]
7. Ezetimibe comparison assay (BALB/c mice): Female BALB/c mice (7–10 weeks old) were fed a rodent chow diet containing Ro 48-8071 fumarate or ezetimibe (20 mg/day/kg bw) for 7–10 days; cholesterol absorption, fecal neutral/acidic sterol excretion, intestinal weight, unesterified cholesterol concentration, and intestinal gene expression (NPC1L1, CYP3A11, CES2A) were measured [4]

1. Ro 48-8071 fumarate was safe at pharmacologically active doses in hamsters, squirrel monkeys and Göttingen miniature pigs; no hepatotoxicity was observed at effective doses, whereas simvastatin caused hepatotoxicity in hamsters at doses >30 μmol/kg/day[1]
2. Ro 48-8071 fumarate did not reduce coenzyme Q10 levels in the liver and heart of hamsters, indicating the absence of mitochondrial toxicity associated with coenzyme Q10 depletion[1]
3. Ro 48-8071 fumarate was non-toxic to thymic nu/nu nude mice carrying PC-3 prostate cancer xenografts: no significant changes in animal weight were observed during treatment (tail vein injection of 5/20 mg/kg); in the 20 mg/kg dose group, 2 out of 12 tumors were completely cleared and no obvious side effects were observed[2]
4. Ro 48-8071 fumarate showed no significant toxicity to nude mice carrying BT-474 breast cancer xenografts: no significant changes in animal body weight were observed during treatment (tail vein injection of 5/10 mg/kg) [3]
5. Ro 48-8071 fumarate (20 mg/day/kg body weight, 16 days) had no significant effect on intestinal histology (H&E staining) and Ki67 expression (proliferation index) in BALB/c mice; no significant changes were observed in the mRNA expression of intestinal proliferation/apoptosis-related genes [4]

[1]. Ro 48-8.071, a new 2,3-oxidosqualene:lanosterol cyclase inhibitor lowering plasma cholesterol in hamsters, squirrel monkeys, and minipigs: comparison to simvastatin. J Lipid Res. 1997 Feb;38(2):373-90.

[2]. Cholesterol biosynthesis inhibitor RO 48-8071 suppresses growth of hormone-dependent and castration-resistant prostate cancer cells. Onco Targets Ther. 2016 May 30;9:3223-32.

[3]. Cholesterol biosynthesis inhibitors as potent novel anti-cancer agents: suppression of hormone-dependent breast cancer by the oxidosqualene cyclase inhibitor RO 48-8071. Breast Cancer Res Treat. 2014 Jul;146(1):51-62.

[4]. Sustained and selective suppression of intestinal cholesterol synthesis by Ro 48-8071, an inhibitor of 2,3-oxidosqualene:lanosterol cyclase, in the BALB/c mouse. Biochem Pharmacol. 2014 Apr 1;88(3):351-63.

Ro 48-8071 fumarate is a fumarate synthase prepared by combining Ro 48-8071 with an equimolar amount of fumaric acid. It is an inhibitor of lanosterol synthase. It functions as an EC 5.4.99.7 (lanosterol synthase) inhibitor and an antitumor drug. It contains one fumarate ion (1-) and one Ro 48-8071 ion (1+).

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1. 2,3-Oxysqualene: Lanosterol cyclase (OSC) is a unique target for cholesterol-lowering drugs; partial OSC inhibition can reduce the synthesis of lanosterol/sterol and stimulate the production of epoxysterol, thereby inhibiting the expression of HMG-CoA reductase and forming a synergistic negative regulatory loop [1]
2. Ro 48-8071 fumarate is a small molecule OSC inhibitor, whose pharmacological properties are completely different from those of statins (HMG-CoA reductase inhibitors): statins can stimulate the expression of liver HMG-CoA reductase/squalene synthase/OSC and reduce the level of coenzyme Q10, while RO has no such effect [1]
3. Cholesterol is an important structural/functional component of cell membrane and a precursor of endogenous steroid hormones, so the cholesterol biosynthesis pathway is an ideal target for endocrine-dependent cancers [2]
4. Ro 48-8071 fumarate 48-8071 is the first OSC inhibitor proven to inhibit the growth of hormone-dependent and castration-resistant cancers. Prostate cancer cells; RO combined with ERβ agonists can enhance its anti-prostate cancer efficacy [2]
5. Rhodamine fumarate 48-8071 exerts its anti-breast cancer effect partly through off-target effects, which can increase the ERβ/ERα ratio in breast cancer cells; statins (fluvastatin, simvastatin) are less effective in reducing breast cancer cell viability and do not induce ERβ [3]
6. Rhodamine fumarate 48-8071 selectively inhibits intestinal cholesterol synthesis in BALB/c mice, and liver cholesterol synthesis returns to baseline levels within 7 days; it does not continuously change systemic cholesterol synthesis or cholesterol absorption rate [4]
7. Rhodamine fumarate 48-8071 can upregulate the mRNA levels of PXR target genes (CYP3A11, CES2A) in the small intestine of mice, but has no significant effect on the mRNA expression of other intestinal cholesterol regulatory genes (such as NPC1L1) [4]

C27H31BRFNO6

564.44

563.131

189197-69-1

Ro 48-8071;161582-11-2

9959583

White to light yellow solid powder

1.2±0.1 g/cm3

522.8±50.0 °C at 760 mmHg

270.0±30.1 °C

0.0±1.4 mmHg at 25°C

1.550

6.24

2

8

14

36

587

0

CN(CCCCCCOC1=CC(=C(C=C1)C(=O)C2=CC=C(C=C2)Br)F)CC=C.C(=C/C(=O)O)\C(=O)O

XCYAYLWZCRGKDS-WLHGVMLRSA-N

InChI=1S/C23H27BrFNO2.C4H4O4/c1-3-14-26(2)15-6-4-5-7-16-28-20-12-13-21(22(25)17-20)23(27)18-8-10-19(24)11-9-18;5-3(6)1-2-4(7)8/h3,8-13,17H,1,4-7,14-16H2,2H3;1-2H,(H,5,6)(H,7,8)/b;2-1+

(4-bromophenyl)-[2-fluoro-4-[6-[methyl(prop-2-enyl)amino]hexoxy]phenyl]methanone;(E)-but-2-enedioic acid

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Solubility in Formulation 1: ≥ 2.5 mg/mL (4.43 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (4.43 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (4.43 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 4: 12.5 mg/mL (22.15 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication (<60°C).

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 (Please use freshly prepared in vivo formulations for optimal results.)