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].

---

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].

---

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.

---

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).

---

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).

---

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.

---

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 after oral administration, with a slow accumulation period following multiple doses. [Label] In healthy male subjects, the mean bioavailability of oral finasteride was 65% at a 1 mg dose and 63% at a 5 mg dose, with a bioavailability range of 26% to 170% for a 1 mg dose and 34% to 108% for a 5 mg dose. Food intake has been reported not to affect the oral bioavailability of this drug. The mean peak plasma concentration (Cmax) is 37 ng/mL (range: 27–49 ng/mL), reaching its peak 1–2 hours after administration. The AUC (0–24 hr) is 53 ng·hr/mL (range: 20–154 ng·hr/mL). Higher plasma concentrations and AUCs have been reported in elderly male patients aged 70 years and older. In healthy subjects, approximately 32–46% of the total oral dose of finasteride is excreted in the urine as metabolites, and approximately 51–64% in the feces. Urinary excretion is expected to be reduced in patients with renal insufficiency, while fecal excretion is expected to be increased. The steady-state volume of distribution is 76 liters, ranging from 44 to 96 liters. Studies have shown that finasteride can cross the blood-brain barrier, but does not appear to preferentially distribute in the cerebrospinal fluid. It is currently unknown whether finasteride is secreted into human breast milk. In healthy young subjects (n=15), the mean plasma clearance of finasteride was 165 mL/min, ranging from 70 to 279 mL/min. Metabolisms/Metabolites Finasteride is primarily metabolized extensively in the liver by cytochrome P450 3A4 (CYP3A4) enzymes, producing tert-butyl side-chain monohydroxylated and monocarboxylic acid metabolites. These metabolites retain less than 20% of the pharmacological activity of the parent compound.
The known human metabolites of finasteride include N-(1-hydroxy-2-methylpropyl-2-yl)-9a,11a-dimethyl-7-oxo-1,2,3,3a,3b,4,5,5a,6,9b,10,11-dodecanoindo[5,4-f]quinoline-1-carboxamide.
The drug is extensively metabolized in the liver via CYP3A4. Two metabolites have been identified, with activity less than 20% of that of finasteride.
Elimination pathway: In humans (n = 6), after oral administration of 14C-finasteride, an average of 39% (range: 32% to 46%) of the dose is excreted in the urine as metabolites; 57% (range: 51% to 64%) is excreted in the feces. Urinary excretion of metabolites is reduced in patients with renal impairment. This reduction is associated with increased fecal excretion of metabolites.
Half-life: 4.5 hours (range: 3.3–13.4 hours)

---

Biological half-life
In healthy young subjects taking finasteride, the mean elimination half-life in plasma is 6 hours, ranging from 3 to 16 hours. In elderly patients aged 70 years and older, the half-life is prolonged to 8 hours.

Hepatotoxicity
Finasteride was associated with a low incidence of elevated serum transaminase levels, which was not higher than in the placebo group in controlled trials. These elevations were transient, rarely requiring dose adjustments, and occurred at both the 5 mg dose for treating benign prostatic hyperplasia and the 1 mg dose for promoting hair growth. Transient elevations of serum enzymes during finasteride treatment have been reported in the literature, but no clinically significant liver injury has been observed. Probability Score: E (Unlikely to be the cause of clinically significant liver injury). Pregnancy and Lactation Effects ◈ What is Finasteride? Finasteride is a medication used to treat male pattern baldness and benign prostatic hyperplasia (prostate enlargement). Oral finasteride (oral tablets) is approved by the U.S. Food and Drug Administration (FDA) for use in men. Finasteride is not approved for use in women, but has been used "off-label" for the treatment of female pattern baldness and hirsutism (e.g., excessive hair growth on the face, chest, and back). Some brand names for finasteride include Propecia® and Proscar®. Topical finasteride (for skin) is not approved by the US FDA but has been used to treat male and female pattern hair loss. This information sheet focuses on the use of oral finasteride. No form of finasteride is recommended for pregnant women.
◈ I am taking finasteride, but I want to stop before I get pregnant. How long will this drug stay in my body?
Everyone metabolizes drugs at different rates. For healthy adults, it takes an average of up to 2 days for most of the finasteride to be eliminated from the body.
◈ I am taking finasteride. Will taking finasteride affect my ability to get pregnant?
It is currently unclear whether finasteride affects pregnancy. Some people taking finasteride have reported decreased libido (low libido).
◈ I just found out I'm pregnant. Should I stop taking finasteride?
It is not recommended to take finasteride during pregnancy. If you are taking finasteride and find out you are pregnant, contact your healthcare provider to discuss your medication use.
◈ Does taking finasteride increase the risk of miscarriage?
Miscarriage is common and can occur in any pregnancy for many reasons. There is currently no research indicating that taking finasteride increases the risk of miscarriage.
◈ Does taking finasteride increase the risk of birth defects?
There is a 3-5% risk of birth defects in each pregnancy. This is called background risk. There are currently no human studies confirming whether finasteride increases the risk of birth defects. Animal studies have shown that exposure to high doses of finasteride during fetal sex organ development (8 to 12 weeks of gestation) may increase the risk of certain sex organ birth defects in male fetuses. Defects reported in animal studies include hypospadias (the opening of the penis is located on the ventral side of the penis rather than the tip), a shortened anal-genital distance (anogenital distance), and reduced weight of the prostate and seminal vesicles (the glands that produce semen).
◈ If I am exposed to or handle finasteride tablets during pregnancy, will it increase the risk of birth defects?
For safety reasons, pregnant women are advised not to handle crushed or broken finasteride tablets. Uncrushed or unbroken tablets should be coated to prevent contact with finasteride during normal handling. If you have handled or handled crushed or broken finasteride tablets, wash your hands. It is unlikely that the medication will cause significant skin penetration problems. Personnel who need to handle finasteride for work purposes should wear gloves, clean surfaces that have come into contact with the tablets, and wash their hands. Workers should discuss proper handling and storage methods with an occupational safety officer. For more information on workplace exposure, see MotherToBaby's fact sheet: https://mothertobaby.org/fact-sheets/reproductive-hazards-workplace/.
◈ Does taking finasteride during pregnancy increase the risk of other pregnancy-related problems?
Currently, there are no human studies confirming that finasteride increases the risk of pregnancy-related problems such as preterm birth (delivery before 37 weeks of gestation) or low birth weight (birth weight less than 5 pounds 8 ounces [2500 grams]). Animal studies have shown that exposure to finasteride during pregnancy may increase the risk of preterm birth and may affect the fetal ability to descend the testes into the correct position in the scrotum (the skin sac under the penis). This process, called testicular descent, usually occurs spontaneously in most males shortly after birth.
◈ Will taking finasteride during pregnancy affect a child's future behavior or learning abilities?
Currently, there are no human studies confirming whether finasteride causes behavioral or learning problems in children. One animal study reported that finasteride use during pregnancy may affect memory in some offspring.
◈ Taking finasteride while breastfeeding:
Currently, there are no studies on taking finasteride while breastfeeding. There is also no information on whether it passes into breast milk. Be sure to consult your healthcare provider about all questions regarding breastfeeding.
◈ If a man is taking finasteride, should he stop taking it before trying to get his partner pregnant?
Men taking finasteride should discuss the benefits of taking the medication and the potential adverse effects of stopping it with their healthcare provider before deciding to discontinue treatment.
◈ Will men taking finasteride affect their fertility (their ability to impregnate their partner) or increase the risk of birth defects in the fetus if their partner becomes pregnant?
It has been reported that men taking finasteride may experience sexual dysfunction. Men taking finasteride may also experience subtle changes in their semen, such as a decrease in sperm count. Sperm count improves after discontinuation of the drug. A rat study showed that male rats taking finasteride did not have an increased chance of birth defects in their offspring after mating with female rats. There have been concerns that unprotected sex during the critical period of pregnancy (weeks 8 to 12 of gestation, the critical period for the development of sex organs) might increase the chance of male infants having sex defects. However, the amount of finasteride in semen is very low. If the fetus is only exposed to the drug through vaginal intercourse via semen, the amount of finasteride in the semen is not expected to be sufficient to cause problems for the developing fetus. There are case reports of fathers being exposed to finasteride before or during pregnancy but still successfully delivering full-term babies without any reported birth defects. In general, paternal or sperm donor exposure to finasteride is unlikely to increase pregnancy risk. For more information, please refer to MotherToBaby's "Paternal Exposure" information sheet at https://mothertobaby.org/fact-sheets/paternal-exposures-pregnancy/.

---

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 anti-androgen compound that works by inhibiting the enzyme responsible for the biosynthesis of dihydrotestosterone (DHT), thereby suppressing DHT production in male serum and the prostate. Serum DHT concentrations are expected to decrease rapidly within 8 hours of the first dose, reaching maximum efficacy. In a 4-year study, a single oral dose of 5 mg finasteride in one man resulted in a approximately 70% reduction in serum DHT concentration and a 10-20% increase in median circulating testosterone levels within the physiological range. In a double-blind, placebo-controlled study, finasteride reduced prostate DHT levels by 91.4%, but because circulating testosterone is also converted to DHT by type 1 isoenzymes expressed in other tissues, finasteride is not expected to reduce DHT levels to castration levels. DHT levels are expected to return to normal within 14 days after discontinuation of the drug. In a study of men with benign prostatic hyperplasia prior to prostatectomy, the finasteride treatment group showed an approximately 80% reduction in DHT levels in the surgically removed prostate tissue compared to the placebo group. While finasteride can reduce prostate volume by 20%, this may not be strongly correlated with symptom improvement. Finasteride has been reported to be more effective in men with enlarged prostate volumes (>25 mL), who are at the highest risk of disease progression. In a phase III clinical trial, oral finasteride treatment of male pattern baldness resulted in 66% and 83% of participants, respectively, experiencing improved hair growth and prevention of further hair loss during the two-year treatment period. These efficacy rates were significantly higher in the treatment group than in the placebo group. Following finasteride administration, dihydrotestosterone (DHT) levels in the scalp decreased by more than 60%, indicating that DHT in the scalp originates from both local DHT production and circulating DHT. Finasteride's effect on scalp DHT may be due to its dual influence on both local hair follicle DHT levels and serum DHT levels. Early clinical observations and controlled studies suggest that finasteride may reduce prostate bleeding. Finasteride is a competitive, specific inhibitor that inhibits type II 5α-reductase. Type II 5α-reductase is a nucleobinding intracellular steroid enzyme, primarily located in prostate stromal cells, that converts the androgen testosterone into the more potent metabolite 5α-dihydrotestosterone (DHT). DHT is considered the main androgen promoting prostate development and enlargement. After accumulating in the prostate, it acts as a hormonal mediator of proliferation. Compared to testosterone, dihydrotestosterone (DHT) has a higher affinity for androgen receptors in the prostate. DHT regulates genes responsible for cell proliferation by acting on androgen receptors. Type II 5α-reductase isoenzymes, along with type I 5α-reductase, are responsible for DHT production and are mainly found in the prostate, seminal vesicles, epididymis, hair follicles, and liver. Although finasteride has a 100-fold higher selectivity for type II 5α-reductase than for type I isoenzyme, long-term use of this drug may have some impact on type I 5α-reductase, which is mainly expressed in sebaceous glands in most areas of the skin, including the scalp, and in the liver. Studies have proposed that type I and type II 5α-reductases are responsible for generating one-third and two-thirds of the circulating dihydrotestosterone (DHT), respectively. Finasteride's mechanism of action involves forming a stable complex with type II 5α-reductase, preferentially inhibiting this enzyme both in vitro and in vivo. Finasteride is selective, exhibiting 100-fold higher selectivity for human type II 5α-reductase than for type I. Inhibition of type II 5α-reductase blocks the peripheral conversion of testosterone to DHT, significantly reducing serum and tissue DHT concentrations, resulting in a slight to moderate increase in serum testosterone levels and a significant increase in prostate testosterone concentration. Since DHT appears to be the primary androgen stimulating prostate growth, a decrease in DHT concentration leads to a reduction in prostate volume (approximately 20-30% reduction after 6-24 months of continuous treatment). Studies have also shown that elevated DHT levels can enhance prostaglandin D2 transcription, thereby promoting the proliferation of prostate cancer cells. The mechanism of action of finasteride in patients with androgenetic alopecia is not fully understood, but studies have shown that finasteride can reduce scalp DHT concentrations to normal hair follicle levels, lower serum DHT levels, promote hair growth, and slow hair loss. Another study suggests that finasteride may reduce prostate bleeding by inhibiting vascular endothelial growth factor (VEGF) in the prostate, leading to prostate atrophy and programmed cell death. This may make the drug beneficial for patients with idiopathic prostate bleeding, bleeding during anticoagulation therapy, or bleeding after instrumentation procedures.

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.

---

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).

View More

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)

---

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).

View More

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

---

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.

---

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