Type II 5α-reductase （IC50: 4.2 nM)

In PC-3 cells, finasteride (10 μM; 6–24 hours) stimulates the expression of the proteins Nrf2 and HO-1 [2]. In crustacean shrimp, finasteride decreases the conversion of [3H]testosterone (T) to [3H]dihydrotestosterone (DHT) [1].

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A number of naturally-occurring or synthetic chemicals have been reported to exhibit prostate chemopreventive effects. Synthetic 5α-reductase (5-AR) inhibitors, e.g. finasteride and durasteride, gained special interests as possible prostate chemopreventive agents. Indeed, two large-scale epidemiological studies have demonstrated that finasteride or durasteride significantly reduced the incidence of prostate cancer formation in men. However, these studies have raised an unexpected concern; finasteride and durasteride increased the occurrence of aggressive prostate tumor formation. In the present study, researchers have observed that treatment of finasteride did not affect the growth of androgen-refractory PC-3 prostate cancer cells. Finasteride also failed to induce apoptosis or affect the expression of proto-oncogenes in PC-3 cells. Interestingly, it was found that treatment of finasteride induced the expression of Nrf2 and HO-1 proteins in PC-3 cells. In particular, basal level of Nrf2 protein was higher in androgen-refractory prostate cancer cells, e.g. DU-145 and PC-3 cells, compared with androgen-responsive prostate cancer cells, e.g. LNCaP cells. Also, treatment of finasteride resulted in a selective induction of Nrf2 protein in DU-145 and PC-3 cells, but not in LNCaP cells. In view of the fact that upregulation of Nrf2-mediated phase II cytoprotective enzymes contribute to attenuating tumor promotion in normal cells, but, on the other hand, confers a selective advantage for cancer cells to proliferate and survive against chemical carcinogenesis and other forms of toxicity, researchers propose that finasteride-mediated induction of Nrf2 protein might be responsible, at least in part, for an increased risk of high-grade prostate tumor formation in men.[2]

In dogs with BPH, finasteride (0.1–0.5 mg/kg; administered orally once daily for 16 weeks) lowers the size of the prostate without negatively impacting the quality of the semen or the levels of testosterone in the blood [3].

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Finasteride significantly decreased prostatic diameter (mean percentage decrease, 20%), prostatic volume (mean percentage decrease, 43%), and serum DHT concentration (mean percentage decrease, 58%). Finasteride decreased semen volume but did not adversely effect semen quality or serum testosterone concentration. No adverse effects were reported by owners of dogs in the study. Conclusions and clinical relevance: Results suggest that finasteride can be used to reduce prostatic size in dogs with BPH without adversely affecting semen quality or serum testosterone concentration. [3]

In order to develop the treatment for 5α-DHT associated diseases such as BPH and PCa, a simple test system has been required to screen for 5α-SR inhibitors. Because of its simplicity and high sensitivity, the present method is also applicable to the simple test system for screening 5α-SR inhibitors. After confirming that finasteride showed no effect on the enzyme cycling of 5α-DHT, we performed the inhibition experiments by finasteride of rat liver and prostate microsomal 5α-SR. From the results, the concentrations of finasteride required to inhibit 5α-SR activity by 50% (IC50) were estimated to be 21 nM for liver 5α-SR and 20 nM for prostate 5α-SR, respectively. The inhibitions of rat 5α-SR1 and 5α-SR2 by fenasteride have been investigated by using COS cells transiently expressing 5α-SR1 and 5α-SR2. The IC50 values of finasteride to 5α-SR1 and 5α-SR2 were evaluated to be and 5.2 nM respectively in whole cell assay, whereas those were 13 and 1.0 nM respectively in the assay with crude enzyme preparations.21 The IC50 value of finasteride to rat 5α-SR in prostate microsomes was also evaluated to be 11 nM by Häusler et al., 13 nM by Igarashi et al. and 237 nM by Mitamura et al. The reported IC50 values of fenasteride to rat 5α-SR in prostate homogenate were in the range from 6.8 to 147 nM. The reason for such a difference may be related to differences in experimental conditions of enzyme activity evaluation such as pH, testosterone concentration and enzyme preparation.

Western Blot Analysis[2]
Cell Types: PC-3, DU-145, and LNCaP cells
Tested Concentrations: 10 μM
Incubation Duration: 6, 12, 24 h
Experimental Results: Increased the expression of HO-1 protein in a time-dependent manner in PC-3 cells. Induced the expression of Nrf2 protein in DU-145 and PC-3 cells, but not in LNCaP cells.

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Trypan-blue exclusion assay [2]
PC-3 cells were seeded in 6-well plates at a density of 1×105 per well. Following an exposure to finasteride for 24 h and 48 h, cells were collected by trypsinization, followed by centrifugation at 1,000 g for 5 min. Collected cells were rinsed with ice-cold phosphate-buffer saline (PBS) solution (pH 7.4) 3 times and mixed with 100 μl of PBS together with an equal amount of 0.4% trypan blue reagent. After counting viable cell numbers that excluded trypan blue reagent by hemacytometer, total number of viable cells was calculated by doubling a dilution factor (×2).

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Western blot analysis [2]
For preparation of whole cell lysates, cells were harvested in whole cell lysis buffer [10 mmol/L Tris-HCl (pH 7.9), 250 mmol/L NaCl, 30 mmol/L sodium bisphosphate, 50 mmol/L sodium fluoride, 0.5% Triton X-100, 10% glycerol, 1×proteinase inhibitor mixture,] for 30 min on ice. Lysates were then collected by centrifugation at 14,800 g for 30 min. Protein concentrations were determined by the BCA protein assay kit. Aliquots of supernatant, containing 30 mg proteins were boiled in 1× SDS sample loading buffer for 2 min and resolved using 12% SDS-PAGE. Proteins in SDS-polyacrylamide gel were transferred to polyvinylidene difluoride (PVDF) membrane. The membrane was blocked with 5% fat-free milk in PBS-Tween 20 (PBST, 0.1% Tween 20) at room temperature for 2 h. The membrane was then probed with primary antibodies (1:1,000) in PBS overnight at 4℃. Blots were rinsed with PBST (PBS with 0.1% Tween-20) three times and then incubated with 1:5,000 dilution of horseradish peroxidase–conjugated second antibody at room temperature for 1 h. The blots were washed in PBST buffer for 5 min thee times and the transferred protein was visualized, using the enhanced chemiiluminescence (ECL).

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Measurement of dual luciferase activity [2]
U2OS cells were plated in six-well plates and allowed to grow around 70% confluency. 0.1 mg COX-2-, MMP2- and NF-kB-promoter-driven firefly luciferase constructs were cotransfected with 0.1 μg Renilla luciferase plasmid, using lipofectamine reagent. After transfection, cells were treated with DMSO or finasteride for additional 48 h. Cells were then collected and the dual luciferase activity was measured by the GLOMAX Multi-detection system. The measured firefly luciferase activity was normalized against the measured Renilla luciferase activity and the resulting value was expressed as a fold induction over the control. Values are expressed as mean ± SD of experiments and statistical analysis was performed, using Student t-test with n=6.

Animal/Disease Models: Male dog (2.7-11 years old; 10.3-49 kg) with spontaneous BPH [3]
Doses: 0.1-0.5 mg/kg
Route of Administration: Orally one time/day for 16 weeks
Experimental Results: Prostate diameter reduction ( 20%), prostate volume (43%) and serum DHT concentration (58%). Semen volume is diminished but does not adversely affect semen quality or serum testosterone concentrations. No adverse effects on dogs.

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Objective: To determine the effect of the 5alpha-reductase inhibitor finasteride on prostatic diameter and volume, semen quality, and serum dihydrotestosterone (DHT) and testosterone concentrations in dogs with spontaneous benign prostatic hypertrophy (BPH).
Design: Double-blind placebo-controlled trial.
Animals: 9 dogs with BPH.
Procedure: Five dogs were treated with finasteride for 16 weeks (0.1 to 0.5 mg/kg [0.05 to 0.23 mg/lb] of body weight, PO, q 24 h); the other 4 received a placebo. Prostatic diameter, measured radiographically, prostatic volume, measured ultrasonographically, semen quality, and serum DHT and testosterone concentrations were evaluated before and during treatment. After receiving the placebo for 16 weeks, the 4 control dogs were treated with finasteride for 16 weeks, and evaluations were repeated.[3]

Absorption, Distribution and Excretion
Finasteride is well absorbed following oral administration and displays a slow accumulation phase after multiple dosing.[lablel] In healthy male subjects receiving oral finasteride, the mean oral bioavailability was 65% for 1 mg finasteride and 63% for 5 mg finasteride, and the values ranged from 26 to 170% for 1 mg dose and from 34 to 108% for 5 mg dose, respectively. It is reported that food intake does not affect the oral bioavailability of the drug. The peak plasma concentrations (Cmax) averaged 37 ng/mL (range, 27-49 ng/mL) and was reached 1-2 hours post administration. The AUC(0-24 hr) was 53 ngxhr/mL (range, 20-154 ngxhr/mL). The plasma concentrations and AUC are reported to be higher in elderly male patients aged 70 years or older.
In healthy subjects, about 32-46% of total oral dose of finasteride was excreted in the urine in the form of metabolites while about 51-64% of the dose was excreted in the feces. In patients with renal impairment, the extent of urinary excretion of finasteride is expected to be decreased while the fecal excretion is increased.
The volume of distribution is 76 L at steady state, ranging from 44 to 96 L. Finasteride has been shown to cross the blood brain barrier but does not appear to distribute preferentially to the CSF. It is not known whether finasteride is excreted in human milk.
In healthy young subjects (n=15), the mean plasma clearance of finasteride was 165 mL/min with the range between 70 and 279 mL/min.

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Metabolism / Metabolites
Finasteride undergoes extensive hepatic metabolism predominantly mediated by the cytochrome P450 3A4 (CYP3A4) enzyme to form the t-butyl side chain monohydroxylated and monocarboxylic acid metabolites. Theses metabolites retain less than 20% of the pharmacological activity of the parent compound.
Finasteride has known human metabolites that include N-(1-Hydroxy-2-methylpropan-2-yl)-9a,11a-dimethyl-7-oxo-1,2,3,3a,3b,4,5,5a,6,9b,10,11-dodecahydroindeno[5,4-f]quinoline-1-carboxamide.
Drug is extensively metabolized, primarily in the liver via CYP3A4. Two metabolites have been identified with дЉ_20% of the activity of finasteride.
Route of Elimination: Following an oral dose of 14C-finasteride in man (n = 6), a mean of 39% (range, 32 to 46%) of the dose was excreted in the urine in the form of metabolites; 57% (range, 51 to 64%) was excreted in the feces. Urinary excretion of metabolites was decreased in patients with renal impairment. This decrease was associated with an increase in fecal excretion of metabolites.
Half Life: 4.5 hours (range 3.3-13.4 hours)

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Biological Half-Life
In healthy young subjects receiving finasteride, the mean elimination half-life in plasma was 6 hours ranging from 3 to 16 hours. In elderly patients over the age of 70 years, the half-life is prolonged to 8 hours.

Hepatotoxicity
Finasteride has been associated with a low rate of serum aminotransferase elevations that, in controlled trials, was no higher than with placebo therapy. These elevations were transient and rarely required dose modification, and have occurred with both the 5 mg dose for prostatic hypertrophy and the 1 mg dose for hair growth. There have been published reports of transient serum enzyme elevations occurring during finasteride therapy, but none of clinically apparent liver injury.
Likelihood score: E (unlikely cause of clinically apparent liver injury).

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Effects During Pregnancy and Lactation
◈ What is finasteride?
Finasteride is a medication that has been used to treat male pattern hair loss and benign prostatic hyperplasia (enlarged prostate). Oral finasteride (a pill taken by mouth) has been approved by the U.S. Food and Drug Administration (FDA) for use in males. Finasteride is not approved for use in females but has been used “off-label” in females to treat hair loss and hirsutism (extra hair growth on areas of the body such as the face, chest, and back). Some brand names for finasteride are Propecia® and Proscar®.Topical finasteride (used on the skin) has not been approved by the U.S. FDA, but has been used to treat male and female pattern hair loss. This fact sheet will focus on the use of oral finasteride. Finasteride, in any form, is not recommended for use by someone who is pregnant.
◈ I am taking finasteride, but I would like to stop taking it before becoming pregnant. How long does the drug stay in my body?
People eliminate medication at different rates. In healthy adults, it takes up to 2 days, on average, for most of the finasteride to be gone from the body.
◈ I take finasteride. Can it make it harder for me to get pregnant?
It is not known if finasteride can make it harder to get pregnant. Some people taking finasteride have reported reduced desire to have sex (low libido).
◈ I just found out I am pregnant. Should I stop taking finasteride?
Finasteride is not recommended for use during pregnancy. If you are taking finasteride and find out that you are pregnant, contact your healthcare provider to talk about your exposure.
◈ Does taking finasteride increase the chance of miscarriage?
Miscarriage is common and can occur in any pregnancy for many different reasons. Studies have not been done to see if taking finasteride could increase the chance of a miscarriage.
◈ Does taking finasteride increase the chance of birth defects?
Every pregnancy starts out with a 3-5% chance of having a birth defect. This is called the background risk. Studies have not been done in humans to see if finasteride increases the chance for birth defects above the background risk.Animal studies have suggested that exposure to large doses of finasteride when the fetal sex organs are developing (8 to 12 weeks of pregnancy) could increase the chance for some birth defects of the sex organs in a male fetus. The animal studies have reported hypospadias (when the opening of the penis is on the underside of the penis instead of at the tip), a shorter distance from the anus to the genitals (anogenital distance), and lower weight of the prostate and seminal vesicles (glands that help make semen).
◈ If I touch or handle finasteride tablets during pregnancy, is there an increased chance for birth defects?
People who are pregnant are told not to handle finasteride tablets that are crushed or broken as a precaution. The coating on uncrushed or unbroken tablets should prevent contact with finasteride during normal handling. If you touch or handle crushed or broken finasteride tablets, wash your hands. It is unlikely that enough of the medication would get through the skin to be a problem.People who are required to work with finasteride as part of their job should wear gloves, clean surface areas where pills are handled, and wash their hands. Workers should discuss proper handling and storage with their occupational safety officers. For more information about workplace exposures, see the MotherToBaby fact sheet here: https://mothertobaby.org/fact-sheets/reproductive-hazards-workplace/.
◈ Does taking finasteride in pregnancy increase the chance of other pregnancy-related problems?
Studies have not been done in humans to see if finasteride increases the chance for pregnancy-related problems such as preterm delivery (birth before week 37) or low birth weight (weighing less than 5 pounds, 8 ounces [2500 grams] at birth).Experimental animal studies suggest that finasteride exposure in pregnancy might increase the chance of preterm delivery and might affect the ability of the baby’s testicles to move down into the proper position in the scrotum (the bag of skin hanging below the penis). This process is called testicular descent and usually happens on its own in most males soon after their birth.
◈ Does taking finasteride in pregnancy affect future behavior or learning for the child?
Studies have not been done in humans to see if finasteride can cause behavior or learning issues for the child. An animal study reported use of finasteride in pregnancy might affect memory in some exposed offspring.
◈ Breastfeeding while taking finasteride:
Finasteride use while breastfeeding has not been studied. No information is available on its transfer into human milk. Be sure to talk to your healthcare provider about all your breastfeeding questions.
◈ If a male is taking finasteride, should they stop taking finasteride before trying to get a partner pregnant?
Males taking finasteride should discuss the benefits of taking the medication and possible harmful effects from not taking it with their healthcare provider before deciding to stop treatment.
◈ If a male takes finasteride, could it affect fertility (ability to get partner pregnant) or increase the chance of birth defects in a partner’s pregnancy?
Problems with sexual function have been reported in males taking finasteride. Some small differences have been seen in the semen of males who take finasteride, such as low sperm counts. Sperm levels improved when the medication was stopped.A study in rats did not show an increased chance for birth defects in the offspring of female rats who had mated with male rats given finasteride.There has been concerns about an increased chance of birth defects involving the sex organs of male babies if a male and female had unprotected sex during the critical time in pregnancy when the sex organs are developing (8 to 12 weeks of pregnancy). However, the amount of finasteride found in semen is small. If fetal exposure to the drug is only through semen with vaginal sex, the amount of finasteride in semen is not expected to be enough to cause a problem for the developing baby. There are case reports of pregnancies with documented paternal exposure to finasteride either before or during pregnancy that resulted in the birth of full-term infants without reported birth defects. In general, exposures that fathers or sperm donors have are unlikely to increase the risks to a pregnancy. For more information, please see the MotherToBaby fact sheet Paternal Exposures at https://mothertobaby.org/fact-sheets/paternal-exposures-pregnancy/.

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Protein Binding
Approximately 90% of circulating finasteride is bound to plasma proteins.

[1]. Steroid 5alpha-reductase inhibitors. Mini Rev Med Chem. 2003 May;3(3):225-37.

[2]. Finasteride Increases the Expression of Hemoxygenase-1 (HO-1) and NF-E2-Related Factor-2 (Nrf2) Proteins in PC-3 Cells: Implication of Finasteride-Mediated High-Grade Prostate Tumor Occurrence. Biomol Ther (Seoul). 2013 Jan;21(1):49-53.

[3]. Effects of finasteride on size of the prostate gland and semen quality in dogs with benign prostatic hypertrophy. J Am Vet Med Assoc. 2001 Apr 15;218(8):1275-80.

Finasteride is an antiandrogenic compound that works by suppressing the production of serum and intraprostatic dihydrotestosterone (DHT) in men via inhibiting the enzyme responsible for the biosynthesis of DHT. The maximum effect of a rapid reduction in serum DHT concentration is expected to be observed 8 hours following administration of the first dose. In a single man receiving a single oral dose of 5 mg finasteride for up to 4 years, there was a reduction in the serum DHT concentrations by approximately 70% and the median circulating level of testosterone increased by approximately 10-20% within the physiologic range. In a double-blind, placebo-controlled study, finasteride reduced intraprostatic DHT level by 91.4% but finasteride is not expected to decrease the DHT levels to castrate levels since circulating testosterone is also converted to DHT by the type 1 isoenzyme expressed in other tissues. It is expected that DHT levels return to normal within 14 days upon discontinuation of the drug. In a study of male patients with benign prostatic hyperplasia prior to prostatectomy, the treatment with finasteride resulted in an approximate 80% lower DHT content was measured in prostatic tissue removed at surgery compared to placebo. While finasteride reduces the size of the prostate gland by 20%, this may not correlate well with improvement in symptoms. The effects of finasteride are reported to be more pronounced in male patients with enlarged prostates (>25 mL) who are at the greatest risk of disease progression. In phase III clinical studies, oral administration of finasteride in male patients with male pattern hair loss promoted hair growth and prevented further hair loss by 66% and 83% of the subjects, respectively, which lasted during two years' treatment. The incidences of these effects in treatment groups were significantly higher than that of the group receiving a placebo. Following finasteride administration, the levels of DHT in the scalp skin was shown to be reduced by more than 60%, indicating that the DHT found in scalp is derived from both local DHT production and circulating DHT. The effect of finasteride on scalp DHT is likely seen because of its effect on both local follicular DHT levels as well as serum DHT levels.. There is evidence from early clinical observations and controlled studies that finasteride may reduce bleeding of prostatic origin.

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Finasteride acts as a competitive and specific inhibitor of Type II 5α-reductase, a nuclear-bound steroid intracellular enzyme primarily located in the prostatic stromal cell that converts the androgen testosterone into the more active metabolite, 5α-dihydrotestosterone (DHT). DHT is considered to be the primary androgen playing a role in the development and enlargement of the prostate gland. It serves as the hormonal mediator for the hyperplasia upon accumulation within the prostate gland. DHT displays a higher affinity towards androgen receptors in the prostate gland compared to testosterone and by acting on the androgen receptors, DHT modulates genes that are responsible for cell proliferation. Responsible for the production of DHT together with type I 5α-reductase, the type II 5α-reductase isozyme is primarily found in the prostate, seminal vesicles, epididymides, and hair follicles as well as liver. Although finasteride is 100-fold more selective for type II 5α-reductase than for the type I isoenzyme, chronic treatment with this drug may have some effect on type I 5α-reductase, which is predominantly expressed in sebaceous glands of most regions of skin, including the scalp, and liver. It is proposed that the type I 5α-reductase and type II 5α-reductase is responsible for the production of one-third and two-thirds of circulating DHT, respectively. The mechanism of action of Finasteride is based on its preferential inhibition of Type II 5α-reductase through the formation of a stable complex with the enzyme _in vitro_ and _in vivo_. Finasteride works selectively, where it preferentially displays a 100-fold selectivity for the human Type II 5α-reductase over type I enzyme. Inhibition of Type II 5α-reductase blocks the peripheral conversion of testosterone to DHT, resulting in significant decreases in serum and tissue DHT concentrations, minimal to moderate increase in serum testosterone concentrations, and substantial increases in prostatic testosterone concentrations. As DHT appears to be the principal androgen responsible for stimulation of prostatic growth, a decrease in DHT concentrations will result in a decrease in prostatic volume (approximately 20-30% after 6-24 months of continued therapy). It is suggested that increased levels of DHT can lead to potentiated transcription of prostaglandin D2, which promotes the proliferation of prostate cancer cells. In men with androgenic alopecia, the mechanism of action has not been fully determined, but finasteride has shown to decrease scalp DHT concentration to the levels found in the hairy scalp, reduce serum DHT, increase hair regrowth, and slow hair loss. Another study suggests that finasteride may work to reduce bleeding of prostatic origin by inhibiting vascular endothelial growth factor (VEGF) in the prostate, leading to atrophy and programmed cell death. This may bestow the drug therapeutic benefits in patients idiopathic prostatic bleeding, bleeding during anticoagulation, or bleeding after instrumentation.

C25H40N2O4

432.5961

432.298

222989-99-3

Finasteride;98319-26-7

78357778

Typically exists as solid at room temperature

3

4

2

31

709

7

O=C([C@@]1([H])C([H])([H])C([H])([H])[C@@]2([H])[C@]3([H])C([H])([H])C([H])([H])[C@]4([H])[C@@](C([H])=C([H])C(N4[H])=O)(C([H])([H])[H])[C@@]3([H])C([H])([H])C([H])([H])[C@@]21C([H])([H])[H])N([H])C(C([H])([H])[H])(C([H])([H])[H])C([H])([H])[H].O([H])C(C([H])([H])[H])=O

CYWQSECJQBIRJR-ZNBOUQNXSA-N

InChI=1S/C23H36N2O2.C2H4O2/c1-21(2,3)25-20(27)17-8-7-15-14-6-9-18-23(5,13-11-19(26)24-18)16(14)10-12-22(15,17)4;1-2(3)4/h11,13-18H,6-10,12H2,1-5H3,(H,24,26)(H,25,27);1H3,(H,3,4)/t14-,15-,16-,17+,18+,22-,23+;/m0./s1

(1S,3aS,3bS,5aR,9aR,9bS,11aS)-N-tert-butyl-9a,11a-dimethyl-7-oxo-1,2,3,3a,3b,4,5,5a,6,9b,10,11-dodecahydroindeno[5,4-f]quinoline-1-carboxamide;acetic acid

Finasteride (acetate); Finasteride acetate; 222989-99-3; (1S,3aS,3bS,5aR,9aR,9bS,11aS)-N-tert-butyl-9a,11a-dimethyl-7-oxo-1,2,3,3a,3b,4,5,5a,6,9b,10,11-dodecahydroindeno[5,4-f]quinoline-1-carboxamide;acetic acid; MK-906 acetate;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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