Vitamin B12 (Cyanocobalamin) acts as a cofactor for two key enzymes: 1. Methylmalonyl-CoA mutase (required for the conversion of methylmalonyl-CoA to succinyl-CoA in branched-chain amino acid and odd-chain fatty acid metabolism; no IC50/Ki values reported). 2. Methionine synthase (catalyzes the conversion of homocysteine to methionine, regenerating tetrahydrofolate; no IC50/Ki values reported).

Out of all the B vitamins, vitamin B12 is one. In most cases, it affects DNA synthesis and regulation, but it also plays a role in energy production, fatty acid synthesis (particularly odd chain fatty acid synthesis), and the metabolism of every cell in the human body. Yet, since vitamin B12 is required for the body to produce folate again, folic acid (vitamin B9) in enough amounts can substitute for many, if not all, of the effects of vitamin B12. When the body lacks sufficient folic acid to produce thymine due to methyl trapping, poor synthesis of DNA occurs. Therefore, the majority of symptoms associated with vitamin B12 deficiency are actually symptoms of folate deficiency. This includes all the effects of megaloblastosis and pernicious anemia. All known B12-related deficiency syndromes return to normal when adequate folic acid is available, with the exception of those that are specifically linked to the growth of their respective substrates, homocysteine and methylmalonic acid, and the vitamin B12-dependent enzymes methylmalonyl Coenzyme A mutase and 5-methyltetrahydrofolate-homocysteine methyltransferase (MTR), also called methionine synthase. The reactive C-Co bond in Coenzyme B12 contributes to three main categories of enzyme-catalyzed reactions[1][2].

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- Enzymatic Activity: - Reference [2]: In in vitro assays, Vitamin B12 (as methylcobalamin) is essential for the activity of methionine synthase. The enzyme requires methylcobalamin to transfer a methyl group from methyltetrahydrofolate to homocysteine, forming methionine. Similarly, adenosylcobalamin (a form of B12) is required for methylmalonyl-CoA mutase activity, facilitating the rearrangement of methylmalonyl-CoA to succinyl-CoA. These reactions are critical for proper cellular metabolism but were not quantified with IC50/EC50 values in the review.

- Metabolic Role: - Reference [2]: In animal models, Vitamin B12 deficiency leads to impaired methylmalonyl-CoA mutase activity, causing accumulation of methylmalonic acid and subsequent neurological dysfunction. Methionine synthase deficiency disrupts homocysteine metabolism, leading to hyperhomocysteinemia and DNA hypomethylation. These effects were observed in studies of B12-deficient rats and humans but were not quantified with specific in vivo efficacy metrics (e.g., dose-response curves).

- Methylmalonyl-CoA Mutase Activity Assay: - Reference [2]: The activity of methylmalonyl-CoA mutase is typically measured using radiolabeled substrates. For example, [14C]-methylmalonyl-CoA is incubated with enzyme and adenosylcobalamin in buffer containing MgCl2 and dithiothreitol. The reaction produces [14C]-succinyl-CoA, which is separated by thin-layer chromatography and quantified by scintillation counting. The assay confirms the requirement of adenosylcobalamin for enzyme activity but does not provide IC50 values for B12 itself (as it is a cofactor, not an inhibitor).
- Methionine Synthase Activity Assay: - Reference [2]: Methionine synthase activity is measured by monitoring the conversion of [3H]-homocysteine to [3H]-methionine in the presence of methyltetrahydrofolate and methylcobalamin. The reaction mixture includes Tris-HCl buffer (pH 7.5), EDTA, and reducing agents. The product is separated by ion-exchange chromatography and quantified. Again, no IC50 values for B12 were reported in the review.

Absorption, Distribution and Excretion
Vitamin B12 is quickly absorbed from intramuscular (IM) and subcutaneous (SC) sites of injection; with peak plasma concentrations achieved about 1 hour after IM injection. Orally administered vitamin B12 binds to intrinsic factor (IF) during its transport through the stomach. The separation of Vitamin B12 and IF occurs in the terminal ileum when calcium is present, and vitamin B12 is then absorbed into the gastrointestinal mucosal cells. It is then transported by transcobalamin binding proteins. Passive diffusion through the intestinal wall can occur, however, high doses of vitamin B12 are required in this case (i.e. >1 mg). After the administration of oral doses less than 3 mcg, peak plasma concentrations are not reached for 8 to 12 hours, because the vitamin is temporarily retained in the wall of the lower ileum.
This drug is partially excreted in the urine. According to a clinical study, approximately 3-8 mcg of vitamin B12 is secreted into the gastrointestinal tract daily via the bile. In patients with adequate levels of intrinsic factor, all except approximately 1 mcg is reabsorbed. When vitamin B12 is administered in higher doses that saturate the binding capacity of plasma proteins and the liver, the unbound vitamin B12 is eliminated rapidly in the urine. The body storage of vitamin B12 is dose-dependent.
Cobalamin is distributed to tissues and stored mainly in the liver and bone marrow.
During vitamin loading, the kidney accumulates large amounts of unbound vitamin B12. This drug is cleared partially by the kidney, however, multiligand receptor _megalin_ promotes the reuptake and reabsorption of vitamin B12 into the body,.
IN MICE INJECTED IV WITH VITAMIN B12, THE VITAMIN ACCUMULATED RAPIDLY IN THE PLACENTA & WAS TRANSFERRED SLOWLY TO THE FETUSES. PEAK CONCN IN THE FETUSES WAS REACHED 24 HR AFTER DOSING, & FETAL ACCUMULATION WAS DOSE-DEPENDENT.
IN /MICE/ VITAMIN B12 PRESENTS UNUSUAL PATTERN OF PLACENTAL TRANSFER, FOR EVEN WITH 0.20 UG MATERNAL DOSE AVG FETAL CONCN IS 130 TIMES HIGHER THAN MATERNAL ONE. THIS INDICATES STRONGLY OPERATION OF SPECIFIC TRANSPORT MECHANISM FOR VITAMIN B12, POSSIBLY SIMILAR TO ITS GI ABSORPTION ...
IN RATS, PLACENTAL TRANSFER OF VITAMIN B12 WAS SHOWN TO INCR DURING GESTATION. ALTHOUGH QUANTITY TRANSPORTED EACH DAY WAS PROPORTIONAL TO FETAL WT, THE AMT TRANSPORTED PER G OF PLACENTA INCR TEN-FOLD FROM DAY 10 TO DAY 19.
Vitamin B12 is irregularly absorbed from the distal small intestine following oral administration. Dietary vitamin B12 is protein bound and this bond must be split by proteolysis and gastric acid before absorption. In the stomach, free vitamin B12 is attached to intrinsic factor; intrinsic factor a glycoprotein secreted by the gastric mucosa, is necessary for active absorption of the vitamin from the GI tract. The vitamin B12-intrinsic factor complex passes into the intestine, where much of the complex is transiently retained at specific receptor sites in the wall of the lower ileum before the vitamin B12 portion is absorbed into systemic circulation.
For more Absorption, Distribution and Excretion (Complete) data for CYANOCOBALAMIN (9 total), please visit the HSDB record page.

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Metabolism / Metabolites
Vitamin B12 or cyanocobalamin obtained from food is initially bound by _haptocorrin_, a protein found in the saliva with high affinity for B12. This forms a _haptocorrin-B12_ complex. Cyanocobalamin passes through the stomach and is protected from acid degradation due to its binding to haptocorrin. In the duodenum, pancreatic _proteases_ release cobalamin from the _haptocorrin-B12 complex_ and from other proteins containing protein-bound B12 that have been ingested. Following this, the binding of cobalamin to a second glycoprotein, _intrinsic factor_, promotes its uptake by terminal ileum mucosal cells by a process called _cubilin_/AMN receptor-mediated endocytosis. After absorption into enterocytes, intrinsic factor is broken down in the lysosome, and cobalamin is then released into the bloodstream. The transporter ABCC1, found in the basolateral membrane of intestinal epithelial and other cells, exports cobalamin bound to transcobalamin out of the cell. Cyanocobalamin then passes through the portal vein in the liver, and then reaches the systemic circulation. The active forms of cyanocobalamin are _methylcobalamin_ and _adenosylcobalamin_,.
Vitamin B12 is believed to be converted to coenzyme form in the liver and is probably stored in tissues in this form.
Intracellular vitamin B12 is maintained as two active coenzymes methylcobalamin and deoxyadenasylcobalamin.

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Biological Half-Life
Approximately 6 days (400 days in the liver).
HALF-LIFE OF IV ADMIN CYANOCOBALAMIN IN SERUM IS ABOUT 6 DAYS.

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- Absorption: - Reference [1]: Vitamin B12 absorption requires intrinsic factor (IF) secreted by gastric parietal cells. IF binds B12 in the stomach, and the complex is absorbed in the ileum via cubilin-mediated endocytosis. Oral bioavailability is ~50% for low doses (<1 μg) but decreases to ~1% for high doses (>1 mg).
- Distribution: - Reference [1]: B12 is transported in plasma bound to transcobalamin II (TCII) and stored in the liver (~50% of total body stores).
- Excretion: - Reference [1]: Unabsorbed B12 is excreted in feces; excess absorbed B12 is excreted in urine. The biological half-life is ~3–5 years due to efficient enterohepatic recycling.

Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Vitamin B12 is a normal component of human milk. The recommended daily intake in lactating women is 2.8 mcg and for infants aged 6 months or less is 0.4 mcg. Some authorities recommend 5.5 mcg per day during lactation. Supplementation may be necessary to achieve these recommended daily intakes or to correct a known deficiency. Low doses (1 to 10 mcg) of vitamin B12 found in B complex or prenatal vitamins increase milk levels only slightly. Higher daily doses of 50 to 250 mcg are needed in cases of maternal deficiency. The breastfed infant is not exposed to excessive vitamin B12 in such cases, and their vitamin B12 status should improve if it was previously inadequate.
Poor health outcomes in infants with vitamin B12 deficiency include anemia, abnormal skin and hair development, convulsions, weak muscle tone, failure to thrive, mental developmental delay, and potentially abnormal movements. Well-recognized at risk groups are exclusively breastfed infants of mothers with B12 deficiency due to minimal or no dietary intake of animal products or pernicious anemia caused by a maternal malabsorption of B12. Infant vitamin B12 status can be improved through maternal B12 supplementation during pregnancy and lactation. Deficient mothers who miss the opportunity to supplement during pregnancy should still be encouraged to supplement during early lactation since infant vitamin B12 status correlates with milk vitamin B12 levels in breastfed infants up to 6 months of age. Although there are cases reported of exclusively breastfed infants with vitamin B12 deficiency having biochemical and clinical improvement through adequate maternal supplementation alone, direct supplementation of the infant is recommended when such treatments are available.
◉ Effects in Breastfed Infants
Twelve exclusively breastfed infants between 4 and 11 months of age had biochemical, hematological and clinical findings consistent with vitamin B12 deficiency. Their mothers received a 50 mcg single dose of intramuscular vitamin B12. Within 5 to 8 days after the dose, the infants experienced significantly increased hemoglobin and reticulocyte counts, normoblastic erythropoiesis, improved mental status, regression of abnormal skin pigmentation, and reduction in tremors.
Three hundred sixty-six pregnant women in India received 50 mcg of oral vitamin B12 or placebo capsules once daily beginning during their first trimester of pregnancy and continuing until 6 weeks postpartum. Among 218 infants that underwent neurodevelopment testing at 30 months of age, those born to mothers randomized to vitamin B12 had higher expressive language scores than the placebo group when adjusted for baseline maternal vitamin B12 deficiency. Cognitive, receptive language and motor scores were not different between the two groups. Neurophysiological assessments were then conducted at 6 years of age and there were no differences in the measured brain activity between the two groups.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

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Protein Binding
Very high (to specific plasma proteins called transcobalamins); binding of hydroxocobalamin is slightly higher than cyanocobalamin [FDA label.

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Interactions
ABSORPTION OF VITAMINE B12 FROM THE GI TRACT MAY BE DECR BY AMINOGLYCOSIDE ANTIBIOTICS, COLCHICINE, EXTENTED-RELEASE POTASSIUM PREPN, AMINOSALICYLIC ACID & ITS SALTS, ANTICONVULSANTS (EG, PHENYTOIN, PHENOBARBITAL, PRIMADONE), COBALT IRRADIATION OF THE SMALL BOWEL, & BY EXCESSIVE ALCOHOL INTAKE LASTING LONGER THAN 2 WK.
The gastrointestinal absorption of vitamin B12 can be considerably decreased by oral neomycin. Colchicine administration appears to increase neomycin-induced malabsorption of vitamin B12.
The decreased vitamin B12 absorption induced by aminosalicylic acid may be due to the mild malabsorption syndrome that occurs in some patients treated with aminosalicylic acid (PAS).
Patients with pernicious anemia ... respond poorly to vitamin B12 therapy if chloroamphenicol is given concomitantly.
For more Interactions (Complete) data for CYANOCOBALAMIN (7 total), please visit the HSDB record page.

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Toxicity Summary
Usually, cobalamin toxicity or overdose does not occur, and there is no antidote for cobalamin. Vitamin B12 is used in the body in two forms: Methylcobalamin and 5-deoxyadenosyl cobalamin. The enzyme methionine synthase needs methylcobalamin as a cofactor. This enzyme is involved in the conversion of the amino acid homocysteine into methionine. Methionine in turn is required for DNA methylation. 5-Deoxyadenosyl cobalamin is a cofactor needed by the enzyme that converts L-methylmalonyl-CoA to succinyl-CoA. This conversion is an important step in the extraction of energy from proteins and fats. Furthermore, succinyl CoA is necessary for the production of hemoglobin, the substances that carries oxygen in red blood cells.

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- Acute Toxicity: - Reference [1]: Vitamin B12 has low toxicity. No LD50 has been established in humans. High doses (e.g., 1 mg/day) are generally well-tolerated, with rare reports of allergic reactions (rash, itching) or mild gastrointestinal symptoms.
- Chronic Toxicity: - Reference [1]: Long-term use of high-dose B12 does not cause significant organ toxicity. However, excessive intake may mask folate deficiency or interact with certain medications (e.g., metformin, acid-suppressants).

[1]. http://en.wikipedia.org/wiki/Vitamin_B12
[2]. The many faces of vitamin B12: catalysis by cobalamin-dependent enzymes. Annu Rev Biochem, 2003. 72: p. 209-47.

Therapeutic Uses
Hematinics
Vitamin B12 is used in the treatment of pernicious anemia and other vitamin B12 deficiency states. ... Cyanocobalamin ... usually indicated in patients with malabsorption of vitamin B12, such as those with tropical or nontropical sprue (idiopathic steatorrhea, gluten-induced enteropathy); partial or total gastrectomy; regional enteritis; gastroenterostomy; ileal resection; or malignancies, granulomas, strictures, or anastomoses involving the ileum. When the secretion of intrinsic factor is decreased by lesions that destroy the gastric mucosa (eg, following ingestion of corrosives or in patients with extensive GI neoplasia) or by gastric atrophy secondary to multiple sclerosis, certain endocrine disorders, or iron deficiency, or when antibodies to intrinsic factor are present in gastric juice, absorption of vitamin B12 is decreased and cyanocobalamin ... may be required. Malabsorption of vitamin B12 may also be caused by competition for vitamin B12 by bacteria (blind loop syndrome) or by fish tapeworm, Diphyllobothrium latum, or by admin of certain drugs.
The individual with an uncomplicated pernicious anemia, in which the abnormality is restricted to a mild or moderate anemia ... will respond quite well to the admin of vitamin B12 alone.
... Patients with neurological change or severe leukopenia or thrombocytopenia associated with infection or bleeding require emergency treatment. The older individual with a severe anemia (hematocrit less than 20%) is likely to have tissue hypoxia, cerebrovascular insufficiency, and congestive heart failure. Effective therapy must not wait for detailed diagnostic tests. ... The patient should receive intramuscular injections of 100 ug of cyanocobalamin and 1 to 5 mg of folic acid.
For more Therapeutic Uses (Complete) data for CYANOCOBALAMIN (13 total), please visit the HSDB record page.

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Drug Warnings
Cyanocobalamin injection is extremely safe when given by the intramuscular or deep subcutaneous route, but it should never be given intravenously.
Cyanocobalamin should not be used in patients with early Leber's disease (hereditary optic nerve atrophy), since rapid optic nerve atrophy has been reported following admin of the drug to these patients. Vitamin B12 is contraindicated in patients who have experienced hypersensitivity reactions to the vitamin or to cobalt.
/"SHOTGUN"/ ... VITAMIN THERAPY IN TREATMENT OF ... DEFICIENCY CAN BE DANGEROUS. ... THERE IS DANGER THAT SUFFICIENT FOLIC ACID WILL BE GIVEN TO RESULT IN HEMATOLOGICAL RECOVERY; HOWEVER, THIS MAY MASK CONTINUED VIT-B DEFICIENCY & NEUROLOGICAL DAMAGE WILL DEVELOP OR PROGRESS IF ALREADY PRESENT.
Maternal Medication usually Compatible with Breast-Feeding: B12: Reported Sign or Symptom in Infant or Effect on Lactation: None. /from Table 6/
Serum potassium concn should be monitored during early vitamin B12 therapy & potassium admin is necessary, since fatal hypokalemia could occur upon conversion of megaloblastic anemia to normal erythropoesis with vitamin B12 as a result of increased erythrocyte potassium requirements. Because vitamin B12 deficiency may suppress the signs of polycythemia vera, treatment with cyanocobalamin may unmask this condition. The increase in nucleic acid degradation produced by admin vitamin B12 to vitamin B12- deficient patients could result in gout in susceptible individuals. Therapeutic response to vitamin B12 may be impaired by concurrent infection, uremia, folic acid or iron deficiency, or by drugs having bone marrow suppressant effects. Folic acid should be admin with extreme caution to patients with undiagnosed anemia, since folic acid may obscure the diagnosis of pernicious anemia by alleviating hematologic manifestations of the disease while allowing neurologic complications to progress. This may result in severe nervous system damage before the correct diagnosis is made. Vitamin preparations containing folic acid should be avoided by patients with pernicious anemia because folic acid may actually potentiate neurologic complications of vitamin B12 deficiency. Conversely, doses of cyanocobalamin exceeding 10 micrograms daily may improve folate-deficient megaloblastic anemia and obscure the true diagnosis.

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Pharmacodynamics
**General effects** Cyanocobalamin corrects vitamin B12 deficiency and improves the symptoms and laboratory abnormalities associated with pernicious anemia (megaloblastic indices, gastrointestinal lesions, and neurologic damage). This drug aids in growth, cell reproduction, hematopoiesis, nucleoprotein, and myelin synthesis. It also plays an important role in fat metabolism, carbohydrate metabolism, as well as protein synthesis. Cells that undergo rapid division (for example, epithelial cells, bone marrow, and myeloid cells) have a high demand for vitamin B12. **Parenteral cyanocobalamin effects** The parenteral administration of vitamin B12 rapidly and completely reverses the megaloblastic anemia and gastrointestinal symptoms of vitamin B12 deficiency. Rapid parenteral administration of vitamin B12 in deficiency related neurological damage prevents the progression of this condition. **Nasal spray effects** In 24 vitamin B12 deficient patients who were already stabilized on intramuscular (IM) vitamin B12 therapy, single daily doses of intranasal cyanocobalamin for 8 weeks lead to serum vitamin B12 concentrations that were within the target therapeutic range (>200 ng/L).

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- Acute Toxicity: - Reference [1]: Vitamin B12 has low toxicity. No LD50 has been established in humans. High doses (e.g., 1 mg/day) are generally well-tolerated, with rare reports of allergic reactions (rash, itching) or mild gastrointestinal symptoms.
- Chronic Toxicity: - Reference [1]: Long-term use of high-dose B12 does not cause significant organ toxicity. However, excessive intake may mask folate deficiency or interact with certain medications (e.g., metformin, acid-suppressants).

C63H92CON14O14P

1359.41

1354.567

68-19-9

5311498

Dark red crystals or an amorphous or crystalline red powder
Dark-red crystals or red powder

>300ºC

6.57

9

21

26

93

3220

14

[Co+2].P(=O)(O[H])(O[C@]1([H])[C@@]([H])(C([H])([H])O[H])O[C@@]([H])([C@]1([H])O[H])N1C([H])=NC2C([H])=C(C([H])([H])[H])C(C([H])([H])[H])=C([H])C1=2)OC([H])(C([H])([H])[H])C([H])([H])N([H])C(C([H])([H])C([H])([H])[C@@]1(C([H])([H])[H])C2C(C([H])([H])[H])=C3[C@@]([H])(C([H])([H])C([H])([H])C(N([H])[H])=O)C(C([H])([H])[H])(C([H])([H])[H])C(C([H])=C4[C@@]([H])(C([H])([H])C([H])([H])C(N([H])[H])=O)[C@](C([H])([H])[H])(C([H])([H])C(N([H])[H])=O)C(C(C([H])([H])[H])=C5[C@@]([H])(C([H])([H])C([H])([H])C(N([H])[H])=O)[C@](C([H])([H])[H])(C([H])([H])C(N([H])[H])=O)[C@](C([H])([H])[H])([C@@]([H])([C@]1([H])C([H])([H])C(N([H])[H])=O)N=2)[N-]5)=N4)=N3)=O.[C-]([H])([H])[H] |t:73,99,132|

FDJOLVPMNUYSCM-WZHZPDAFSA-L

InChI=1S/C62H90N13O14P.CN.Co/c1-29-20-39-40(21-30(29)2)75(28-70-39)57-52(84)53(41(27-76)87-57)89-90(85,86)88-31(3)26-69-49(83)18-19-59(8)37(22-46(66)80)56-62(11)61(10,25-48(68)82)36(14-17-45(65)79)51(74-62)33(5)55-60(9,24-47(67)81)34(12-15-43(63)77)38(71-55)23-42-58(6,7)35(13-16-44(64)78)50(72-42)32(4)54(59)73-56;1-2;/h20-21,23,28,31,34-37,41,52-53,56-57,76,84H,12-19,22,24-27H2,1-11H3,(H15,63,64,65,66,67,68,69,71,72,73,74,77,78,79,80,81,82,83,85,86);;/q;-1;+3/p-2/t31-,34-,35-,36-,37+,41-,52-,53-,56-,57+,59-,60+,61+,62+;;/m1../s1

cobalt(3+);[(2R,3S,4R,5S)-5-(5,6-dimethylbenzimidazol-1-yl)-4-hydroxy-2-(hydroxymethyl)oxolan-3-yl] [(2R)-1-[3-[(1R,2R,3R,5Z,7S,10Z,12S,13S,15Z,17S,18S,19R)-2,13,18-tris(2-amino-2-oxoethyl)-7,12,17-tris(3-amino-3-oxopropyl)-3,5,8,8,13,15,18,19-octamethyl-2,7,12,17-tetrahydro-1H-corrin-24-id-3-yl]propanoylamino]propan-2-yl] phosphate;cyanide

Docigram; DTXSID7044346; vitamin B12; Coobalamed; Cynobal; B 12, Vitamin; Vitamine B12; ...; 68-19-9; Vitamin B12; Cyanocobalamin

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

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

DMSO : ~20.83 mg/mL (~14.14 mM)
H2O : ~6.25 mg/mL (~4.24 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (1.70 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 (1.70 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: 50 mg/mL (33.94 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.

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