| Size | Price | Stock | Qty |
|---|---|---|---|
| 1mg |
|
||
| 5mg |
|
||
| 10mg |
|
||
| 1g | |||
| Other Sizes |
Purity: =98.79%
| Targets |
- Binds to glucagon-like peptide-1 receptor (GLP-1R) and glucagon receptor (GCGR) (dual agonist); for human GLP-1R, the EC₅₀ is 0.08 nM (measured by cAMP accumulation assay), and for human GCGR, the EC₅₀ is 0.45 nM [1]
- Shows selective activation for GLP-1R and GCGR without significant binding to other related GPCRs (e.g., GIPR); the Ki value for GLP-1R is 0.05 nM, and for GCGR is 0.32 nM (detected by SPR binding assay) [1] - In mouse models, the EC₅₀ for mouse GLP-1R is 0.12 nM and for mouse GCGR is 0.58 nM (measured by cAMP response in transfected cells) [3] |
|---|---|
| ln Vitro |
1. Receptor activation and signal transduction: In CHO-K1 cells stably expressing human GLP-1R, treatment with IBI-362 (Mazdutide; LY-3305677) (0.01-100 nM) induced concentration-dependent cAMP accumulation, with an EC₅₀ of 0.08 nM. In CHO-K1 cells expressing human GCGR, the drug induced cAMP accumulation with an EC₅₀ of 0.45 nM. Western blot analysis showed that 1 nM IBI-362 increased phosphorylation of ERK1/2 (p-ERK1/2) by ~2.5-fold in GLP-1R-expressing cells and ~1.8-fold in GCGR-expressing cells compared to the control group. No significant activation of GIPR (glucose-dependent insulinotropic polypeptide receptor) was observed even at 100 nM [1]
2. Insulin and glucagon secretion regulation in islet cells: Isolated human pancreatic islets were treated with IBI-362 (0.1-10 nM) under high glucose conditions (16.7 mM). At 1 nM, insulin secretion was increased by ~1.8-fold compared to the glucose-only group, while glucagon secretion was inhibited by ~35% compared to the glucose-only group. Under low glucose conditions (3.3 mM), 10 nM IBI-362 did not significantly affect glucagon secretion (no excessive inhibition), indicating glucose-dependent regulation of hormone secretion [1] |
| ln Vivo |
1. Efficacy in db/db mice (type 2 diabetes model): Male db/db mice (8-10 weeks old) were subcutaneously injected with IBI-362 at doses of 0.1, 0.3, and 1.0 mg/kg once weekly for 4 weeks. Compared to the vehicle group: (1) Fasting blood glucose (FBG) at week 4: 0.3 mg/kg group decreased by ~30%, 1.0 mg/kg group decreased by ~45%; (2) Glycated hemoglobin (HbA₁c) at week 4: 1.0 mg/kg group decreased by 1.2% (from 8.5% to 7.3%); (3) Body weight: 1.0 mg/kg group decreased by ~8% (from 52 g to 48 g) at week 4; (4) Energy expenditure (measured by indirect calorimetry): 1.0 mg/kg group increased by ~15% during the dark cycle compared to the vehicle group. Histological analysis of adipose tissue showed that the average size of epididymal white adipocytes in the 1.0 mg/kg group was ~25% smaller than that in the vehicle group [3]
2. Efficacy in phase 1b clinical trial (Chinese patients with type 2 diabetes): A randomized, double-blind, vehicle-controlled trial included 68 Chinese patients with type 2 diabetes (HbA₁c 7.0%-10.0%). Patients were subcutaneously injected with IBI-362 at doses of 0.5, 1.0, 1.5, or 2.0 mg once weekly for 12 weeks. Compared to the vehicle group: (1) HbA₁c change: 1.5 mg group decreased by 1.6% (baseline 8.2% to week 12 6.6%), 2.0 mg group decreased by 1.8%; (2) Fasting plasma glucose (FPG) change: 2.0 mg group decreased by 3.2 mmol/L (baseline 9.5 mmol/L to week 12 6.3 mmol/L); (3) Body weight change: 2.0 mg group decreased by 5.2 kg (baseline 82.5 kg to week 12 77.3 kg); (4) Postprandial 2-hour glucose (PPG): 2.0 mg group decreased by 4.5 mmol/L. No significant increase in fasting glucagon levels was observed in any dose group [2] |
| Enzyme Assay |
1. SPR (Surface Plasmon Resonance) binding assay for GLP-1R/GCGR: Recombinant human GLP-1R and GCGR (extracellular domain) were immobilized on a CM5 sensor chip via amine coupling. IBI-362 was prepared in running buffer (10 mM HEPES pH 7.4, 150 mM NaCl, 0.05% Tween-20) at concentrations of 0.01-10 nM. The drug was injected over the sensor chip at a flow rate of 30 μL/min for 120 seconds (association phase), followed by running buffer for 600 seconds (dissociation phase). The sensorgram data were fitted using a 1:1 binding model to calculate the equilibrium dissociation constant (Ki). The Ki for GLP-1R was 0.05 nM, and for GCGR was 0.32 nM [1]
2. HTRF (Homogeneous Time-Resolved Fluorescence) cAMP assay for receptor activity: CHO-K1 cells expressing human GLP-1R or GCGR were seeded in 384-well plates at 1×10⁴ cells/well and cultured overnight. The medium was replaced with assay buffer (HBSS containing 5 mM HEPES pH 7.4, 0.1% BSA) containing IBI-362 (0.001-100 nM) and a cAMP HTRF detection kit (including cryptate-labeled anti-cAMP antibody and d2-labeled cAMP). The plates were incubated at 37°C for 60 minutes, and fluorescence intensity was measured at 620 nm and 665 nm using a HTRF microplate reader. The ratio of 665 nm/620 nm fluorescence was used to calculate cAMP concentration, and the EC₅₀ was determined by fitting a four-parameter logistic curve [1] |
| Cell Assay |
1. ERK1/2 phosphorylation assay in receptor-expressing cells: CHO-K1 cells stably expressing human GLP-1R or GCGR were seeded in 6-well plates at 5×10⁵ cells/well and serum-starved for 16 hours. Cells were treated with IBI-362 (0.01-10 nM) for 10 minutes, then washed with ice-cold PBS and lysed with RIPA buffer containing protease and phosphatase inhibitors. The cell lysate was centrifuged at 12,000×g for 15 minutes at 4°C, and the supernatant was collected. Equal amounts of protein (30 μg per lane) were separated by 10% SDS-PAGE and transferred to PVDF membranes. Membranes were blocked with 5% non-fat milk in TBST for 1 hour at room temperature, then incubated with primary antibodies against p-ERK1/2, total ERK1/2, and GAPDH (internal control) at 4°C overnight. After washing with TBST, membranes were incubated with HRP-conjugated secondary antibodies for 1 hour at room temperature. Protein bands were visualized using ECL reagent, and gray values were quantified using ImageJ. The relative p-ERK1/2 level was normalized to total ERK1/2 [1]
2. Human islet hormone secretion assay: Human pancreatic islets were isolated and cultured in CMRL 1066 medium containing 10% FBS for 48 hours. Islets (50 islets per well) were seeded in 24-well plates and pre-incubated in Krebs-Ringer bicarbonate buffer (KRBB) containing 3.3 mM glucose for 1 hour. The buffer was replaced with KRBB containing either 3.3 mM glucose (low glucose) or 16.7 mM glucose (high glucose) plus IBI-362 (0.1-10 nM). After incubation at 37°C for 2 hours, the supernatant was collected. Insulin concentration was measured using a human insulin ELISA kit, and glucagon concentration was measured using a human glucagon ELISA kit. Results were normalized to the number of islets per well [1] |
| Animal Protocol |
1. db/db mouse efficacy study: Male db/db mice (8-10 weeks old, body weight 45-55 g) were randomly divided into 4 groups (n=8 per group): vehicle group (0.9% normal saline containing 0.1% Tween-80), IBI-362 0.1 mg/kg group, 0.3 mg/kg group, and 1.0 mg/kg group. The drug was administered via subcutaneous injection once weekly for 4 weeks (injection volume 10 μL/g body weight). Body weight and fasting blood glucose (measured by tail vein blood using a glucometer) were recorded weekly. At the end of the study, mice were anesthetized with isoflurane, and blood was collected via orbital sinus to measure HbA₁c (using a mouse HbA₁c assay kit). Energy expenditure was measured using an indirect calorimetry system (recording O₂ consumption and CO₂ production) for 24 hours at week 3. Epididymal white adipose tissue was collected, fixed in 4% paraformaldehyde, embedded in paraffin, sectioned, and stained with hematoxylin-eosin (HE) to analyze adipocyte size [3]
2. Phase 1b clinical trial protocol (Chinese patients with type 2 diabetes): A total of 68 patients (age 18-65 years, HbA₁c 7.0%-10.0%, BMI 22-35 kg/m²) were randomized into 5 groups (1:1:1:1:1 ratio): vehicle group, IBI-362 0.5 mg group, 1.0 mg group, 1.5 mg group, and 2.0 mg group. The drug was administered via subcutaneous injection (abdomen, thigh, or upper arm) once weekly for 12 weeks. Patients were instructed to fast for ≥8 hours before each injection, and blood samples were collected at baseline, week 4, week 8, and week 12 to measure HbA₁c (by high-performance liquid chromatography), FPG (by glucose oxidase method), and postprandial 2-hour glucose (after a 75 g oral glucose tolerance test). Body weight and vital signs (blood pressure, heart rate) were measured at each visit. Adverse events were recorded throughout the study [2] |
| ADME/Pharmacokinetics |
In Chinese patients with type 2 diabetes (n=13 per dose group) after subcutaneous injection of IBI-362 (0.5-2.0 mg, once weekly): (1) Peak plasma concentration (Cₘₐₓ): Cₘₐₓ in the 2.0 mg group was 32.6 ng/mL (reached at week 12, steady state); (2) Time to peak concentration (Tₘₐₓ): 12-24 hours after each injection; (3) Area under the steady-state concentration-time curve (AUC₀₋₁₆₈ₕ): AUC₀₋₁₆₈ₕ in the 2.0 mg group was 1850 ng·h/mL; (4) Elimination half-life (t₁/₂): ~72 hours (steady state); (5) Clearance (CL/F): 2.0 mg The concentration of the drug was 1.05 L/h in the group; (6) Volume of distribution (Vd/F): 105 L in the 2.0 mg group. No drug accumulation was observed after week 8 [2] - After subcutaneous injection of IBI-362 (1.0 mg/kg) in db/db mice: (1) Cₘₐₓ: 85.3 ng/mL (Tₘₐₓ=6 h); (2) t₁/₂: ~48 h; (3) AUC₀₋₁₂₀ₕ: 3200 ng·h/mL. The drug was mainly distributed in the liver (24-hour concentration of 12.5 ng/g) and adipose tissue (24-hour concentration of 8.3 ng/g), with a lower concentration in brain tissue (24-hour concentration <0.5 ng/g) [3]
|
| Toxicity/Toxicokinetics |
In the Phase 1b clinical trial (Chinese patients): the most common treatment-related adverse events (TRAEs) were gastrointestinal reactions, including nausea (incidence: 38.5% in the 2.0 mg group, 23.1% in the 1.5 mg group, and 7.7% in the placebo group), diarrhea (23.1% in the 2.0 mg group, 15.4% in the 1.5 mg group, and 0% in the placebo group), and vomiting (7.7% in the 2.0 mg group and <5% in other groups). All TRAEs were mild to moderate (grade 1-2) and resolved without intervention. No serious adverse events (grade 3-4) or severe adverse events were reported. No significant changes were observed in liver function (ALT, AST), kidney function (Scr, BUN), or blood lipid levels (TC, TG, LDL-C, HDL-C) from baseline to week 12 [2]
- After subcutaneous injection of IBI-362 (once a week at doses up to 1.0 mg/kg) in db/db mice for 4 weeks: no significant toxic reactions were observed (e.g., weight loss exceeding 10%, behavioral abnormalities, organ hypertrophy/atrophy). Histopathological examination of major organs (liver, kidney, pancreas, heart) revealed no drug-related lesions. No significant changes were observed in serum ALT, AST, Scr, or BUN levels compared to the carrier group [3] - Plasma protein binding: The protein binding rate of IBI-362 in human plasma was 89.2% (measured by ultrafiltration) and in mouse plasma was 85.7% [2][3] |
| References |
|
| Additional Infomation |
1. IBI-362 (madutide; LY-3305677) is a monoclonal dual agonist that simultaneously activates GLP-1R and GCGR receptors. The drug balances the activation of the two receptors through optimized peptide sequence design—GLP-1R mediates glucose-dependent insulin secretion and satiety, while GCGR mediates increased energy expenditure and glycogenolysis (which does not lead to excessive hyperglycemia due to glucose-dependent regulation). This design overcomes the limitations of single GLP-1R agonists (e.g., limited weight loss) and single GCGR agonists (e.g., risk of hyperglycemia) [1]. 2. A phase 1b clinical trial showed that IBI-362 had good efficacy and safety in Chinese patients with type 2 diabetes, with a dose of ≥1.5 mg once weekly significantly reducing HbA1c, fasting blood glucose, and weight. The drug has a long half-life (approximately 72 hours), supporting weekly dosing and thus improving patient compliance [2]. 3. In db/db mice, IBI-362 not only improved glycemic control by increasing insulin secretion and inhibiting glucagon secretion, but also by enhancing insulin sensitivity (as determined by insulin tolerance test: the glucose AUC₀₋₶₀ₘᵢₙ was reduced by 30% in the 1.0 mg/kg group compared to the carrier group). Weight loss was associated with reduced food intake (daily food intake was reduced by 15% in the 1.0 mg/kg group) and increased energy expenditure [3].
|
| Molecular Formula |
C210H322N46O67
|
|---|---|
| Molecular Weight |
4563.06
|
| Exact Mass |
4475.295
|
| CAS # |
2259884-03-0
|
| Related CAS # |
Mazdutide TFA
|
| PubChem CID |
167312357
|
| Sequence |
His-Aib-Gln-Gly-Thr-Phe-Thr-Ser-Asp-Tyr-Ser-Lys-Tyr-Leu-Asp-Glu-Lys-Lys-Ala-Lys(PEG2-PEG2-γ-Glu-Eicosanedioic acid)-Glu-Phe-Val-Glu-Trp-Leu-Leu-Glu-Gly-Gly-Pro-Ser-Ser-Gly-NH2
|
| SequenceShortening |
H-{Aib}-QGTFTSDYSKYLDEKKAK-{AEEA-AEEA-γGlu-Nonadecanoic acid}-EFVEWLLEGGPSSG-NH2
|
| Appearance |
White to off-white solid powder
|
| LogP |
-12.6
|
| Hydrogen Bond Donor Count |
58
|
| Hydrogen Bond Acceptor Count |
70
|
| Rotatable Bond Count |
164
|
| Heavy Atom Count |
317
|
| Complexity |
10500
|
| Defined Atom Stereocenter Count |
31
|
| SMILES |
C[C@H]([C@@H](C(=O)N[C@@H](CC1=CC=CC=C1)C(=O)N[C@@H]([C@@H](C)O)C(=O)N[C@@H](CO)C(=O)N[C@@H](CC(=O)O)C(=O)N[C@@H](CC2=CC=C(C=C2)O)C(=O)N[C@@H](CO)C(=O)N[C@@H](CCCCN)C(=O)N[C@@H](CC3=CC=C(C=C3)O)C(=O)N[C@@H](CC(C)C)C(=O)N[C@@H](CC(=O)O)C(=O)N[C@@H](CCC(=O)O)C(=O)N[C@@H](CCCCN)C(=O)N[C@@H](CCCCN)C(=O)N[C@@H](C)C(=O)N[C@@H](CCCCNC(=O)COCCOCCNC(=O)COCCOCCNC(=O)CC[C@@H](C(=O)O)NC(=O)CCCCCCCCCCCCCCCCCCC(=O)O)C(=O)N[C@@H](CCC(=O)O)C(=O)N[C@@H](CC4=CC=CC=C4)C(=O)N[C@@H](C(C)C)C(=O)N[C@@H](CCC(=O)O)C(=O)N[C@@H](CC5=CNC6=CC=CC=C65)C(=O)N[C@@H](CC(C)C)C(=O)N[C@@H](CC(C)C)C(=O)N[C@@H](CCC(=O)O)C(=O)NCC(=O)NCC(=O)N7CCC[C@H]7C(=O)N[C@@H](CO)C(=O)NCC(=O)N)NC(=O)CNC(=O)[C@H](CCC(=O)N)NC(=O)C(C)(C)NC(=O)[C@H](CC8=CNC=N8)N)O
|
| InChi Key |
XRBYWQZGSZWYEJ-HMQIFOERSA-N
|
| InChi Code |
InChI=1S/C207H317N45O65/c1-116(2)93-144(189(295)230-138(70-76-168(271)272)179(285)221-107-162(264)219-109-166(268)252-86-46-57-157(252)201(307)245-154(110-253)181(287)220-106-159(213)261)234-190(296)145(94-117(3)4)236-194(300)151(100-127-104-218-133-52-37-36-51-131(127)133)240-188(294)142(73-79-171(277)278)233-202(308)174(119(7)8)249-197(303)149(96-123-47-30-28-31-48-123)238-187(293)141(72-78-170(275)276)231-183(289)135(56-41-45-83-215-164(266)113-316-91-90-315-88-85-217-165(267)114-317-92-89-314-87-84-216-160(262)75-69-143(205(311)312)225-161(263)58-34-26-24-22-20-18-16-14-15-17-19-21-23-25-27-35-59-167(269)270)226-177(283)120(9)224-182(288)134(53-38-42-80-208)227-184(290)136(54-39-43-81-209)228-186(292)140(71-77-169(273)274)232-195(301)152(102-172(279)280)241-191(297)146(95-118(5)6)235-192(298)147(98-125-60-64-129(258)65-61-125)237-185(291)137(55-40-44-82-210)229-199(305)155(111-254)244-193(299)148(99-126-62-66-130(259)67-63-126)239-196(302)153(103-173(281)282)242-200(306)156(112-255)246-204(310)176(122(11)257)250-198(304)150(97-124-49-32-29-33-50-124)243-203(309)175(121(10)256)248-163(265)108-222-180(286)139(68-74-158(212)260)247-206(313)207(12,13)251-178(284)132(211)101-128-105-214-115-223-128/h28-33,36-37,47-52,60-67,104-105,115-122,132,134-157,174-176,218,253-259H,14-27,34-35,38-46,53-59,68-103,106-114,208-211H2,1-13H3,(H2,212,260)(H2,213,261)(H,214,223)(H,215,266)(H,216,262)(H,217,267)(H,219,264)(H,220,287)(H,221,285)(H,222,286)(H,224,288)(H,225,263)(H,226,283)(H,227,290)(H,228,292)(H,229,305)(H,230,295)(H,231,289)(H,232,301)(H,233,308)(H,234,296)(H,235,298)(H,236,300)(H,237,291)(H,238,293)(H,239,302)(H,240,294)(H,241,297)(H,242,306)(H,243,309)(H,244,299)(H,245,307)(H,246,310)(H,247,313)(H,248,265)(H,249,303)(H,250,304)(H,251,284)(H,269,270)(H,271,272)(H,273,274)(H,275,276)(H,277,278)(H,279,280)(H,281,282)(H,311,312)/t120-,121+,122+,132-,134-,135-,136-,137-,138-,139-,140-,141-,142-,143-,144-,145-,146-,147-,148-,149-,150-,151-,152-,153-,154-,155-,156-,157-,174-,175-,176-/m0/s1
|
| Chemical Name |
20-[[(1S)-4-[2-[2-[2-[2-[2-[2-[[(5S)-5-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-5-amino-2-[[2-[[(2S)-2-amino-3-(1H-imidazol-4-yl)propanoyl]amino]-2-methylpropanoyl]amino]-5-oxopentanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-hydroxypropanoyl]amino]hexanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-4-carboxybutanoyl]amino]hexanoyl]amino]hexanoyl]amino]propanoyl]amino]-6-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[2-[[2-[(2S)-2-[[(2S)-1-[(2-amino-2-oxoethyl)amino]-3-hydroxy-1-oxopropan-2-yl]carbamoyl]pyrrolidin-1-yl]-2-oxoethyl]amino]-2-oxoethyl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-6-oxohexyl]amino]-2-oxoethoxy]ethoxy]ethylamino]-2-oxoethoxy]ethoxy]ethylamino]-1-carboxy-4-oxobutyl]amino]-20-oxoicosanoic acid
|
| Synonyms |
Mazdutide; IBI362; 2259884-03-0; GTPL13924; IBI-362; compound 1 [US9938335B2];
|
| HS Tariff Code |
2934.99.9001
|
| Storage |
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 (e.g. under nitrogen), avoid exposure to moisture and light. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| Solubility (In Vitro) |
H2O: 22.22 mg/mL (4.87 mM)
|
|---|---|
| Solubility (In Vivo) |
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 Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *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)] Oral Formulations
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 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 0.2192 mL | 1.0958 mL | 2.1915 mL | |
| 5 mM | 0.0438 mL | 0.2192 mL | 0.4383 mL | |
| 10 mM | 0.0219 mL | 0.1096 mL | 0.2192 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
Products are for research use only; We do not sell to patients
Copyright 2020 InvivoChem LLC | All Rights Reserved
COA