E-Selectin (Kd = 0.46 uM; IC50 = 1.75 uM); The primary target of Uproleselan sodium is E-selectin (also known as CD62E), a cell adhesion molecule expressed on vascular endothelial cells . E-selectin is constitutively expressed in the bone marrow microenvironment and is also inducibly expressed during inflammatory responses. In acute myeloid leukemia (AML), alterations in cell-surface glycosylation associated with oncogenesis lead to overexpression of E-selectin ligands (sialyl Lewisˣ) on AML blasts, enhancing binding to E-selectin. This binding directly promotes chemoresistance and survival of AML cells through activation of pro-survival signaling pathways . As a carbohydrate analog of sialyl Lewisˣ, Uproleselan binds to E-selectin with high affinity—Kd of 0.46 µM and IC50 of 1.75 µM by SPR—competitively blocking the interaction between E-selectin and leukemia cells, thereby attenuating the protective effect of the bone marrow microenvironment on AML cells .
Uproleselan targets E-selectin (also known as CD62E or endothelial-leukocyte adhesion molecule 1), a cell adhesion molecule expressed on activated endothelial cells. E-selectin mediates the rolling and adhesion of leukocytes to the endothelium, facilitating their migration into tissues. In the bone marrow microenvironment, E-selectin plays a critical role in the homing and retention of leukemic stem cells, providing a protective niche that supports their survival and chemoresistance. By antagonizing E-selectin, Uproleselan disrupts these interactions, mobilizing leukemic cells from the protective bone marrow niche and sensitizing them to chemotherapy. Uproleselan has a Kd of 0.46 µM and an IC50 of 1.75 µM for E-selectin.

Uproleselan sodium demonstrates high-affinity E-selectin binding activity and functional blocking activity in vitro. Surface plasmon resonance (SPR) assays show that Uproleselan binds to human E-selectin with a Kd of 0.46 µM and IC50 of 1.75 µM, effectively blocking the binding of sialyl Lewisˣ to E-selectin . In functional assays, Uproleselan reverses bone marrow microenvironment-induced chemoresistance in AML cells by disrupting E-selectin-mediated pro-survival signaling pathways . In vitro studies demonstrate that adhesion to E-selectin activates pro-survival signaling pathways in AML cells promoting cell survival; the addition of Uproleselan effectively inhibits this signaling and increases the sensitivity of leukemic cells to chemotherapeutic agents . Furthermore, Uproleselan inhibits cancer (stem) cell quiescence and induces cell maturation, resensitizing leukemia stem cells to chemotherapy . In adhesion assays, Uproleselan at concentrations as low as 100 ng/mL inhibits >90% of KG-1a cell adhesion to recombinant E-selectin.
In vitro, Uproleselan is a potent E-selectin antagonist with a Kd of 0.46 µM and an IC50 of 1.75 µM. The compound blocks E-selectin-mediated adhesion of leukemic cells to endothelial cells, disrupting the bone marrow niche that supports leukemic cell survival. Its potency and selectivity for E-selectin have been characterized in cell adhesion assays using E-selectin-expressing endothelial cells and leukemic cell lines.

Uproleselan (GMI-1271) is a novel E-selectin antagonist that disrupts cell survival pathways, enhances chemotherapy response, improves survival in mouse xenograft and syngeneic models, and decreases chemotherapy toxicity in vivo. A phase 1/2 study evaluated the safety, tolerability, and antileukemic activity of uproleselan (5-20 mg/kg) with MEC (mitoxantrone, etoposide, and cytarabine) among patients with relapsed/refractory (R/R) acute myeloid leukemia (AML). Among the first 19 patients, no dose-limiting toxicities were observed. The recommended phase 2 dose (RP2D) was 10 mg/kg twice daily. An additional 47 patients with R/R AML were treated with uproleselan at the RP2D plus MEC. At the RP2D, the remission rate (complete response [CR]/CR with incomplete count recovery [CRi]) was 41% (CR, 35%), and the median overall survival (OS) was 8.8 months. In a separate cohort, 25 newly diagnosed patients age ≥60 years received uproleselan at the RP2D plus cytarabine and idarubicin (7 + 3). In these frontline patients, the CR/CRi rate was 72% (CR, 52%), and the median OS was 12.6 months. The addition of uproleselan was associated with low rates of oral mucositis. E-selectin ligand expression on leukemic blasts was higher in patients with relapsed vs primary refractory AML and in newly diagnosed older patients with high-risk cytogenetics and secondary AML. In the R/R cohort, E-selectin expression >10% was associated with a higher response rate and improved survival. The addition of uproleselan to chemotherapy was well tolerated, with high remission rates, low induction mortality, and low rates of mucositis, providing a strong rationale for phase 3 randomized confirmatory studies. This trial was registered at www.clinicaltrials.gov as #NCT02306291.[1]

---

Uproleselan sodium demonstrates significant anti-leukemia activity in various in vivo models. In AML mouse xenograft and syngeneic models, Uproleselan combined with chemotherapy (cytarabine) significantly improved mouse survival and reduced the number of chemotherapy-surviving leukemia regenerating cells (LRC) . In an HSCT transplantation model, lethally-irradiated mice reconstituted with hematopoietic stem cells (HSCs) and treated with Uproleselan (40 mg/kg, twice daily) showed median survival extended from 9 days to >30 days, with 80-90% of mice alive at study completion, representing a >233.3% increase in lifespan . In clinical trials, Uproleselan combined with MEC chemotherapy (mitoxantrone, etoposide, and cytarabine) in relapsed/refractory AML patients achieved an overall response rate of 41% (CR 35%) and median overall survival of 8.8 months; in newly diagnosed older AML patients receiving “7+3” induction, the overall response rate was 72% (CR 52%) with median overall survival of 12.6 months .
In vivo, Uproleselan enhances the efficacy of standard chemotherapy in AML and other hematological malignancies. By disrupting E-selectin-mediated interactions, the compound mobilizes leukemic cells from the bone marrow niche, sensitizing them to chemotherapy-induced cell death. Uproleselan has completed Phase II clinical trials, with Phase III studies ongoing for the treatment of AML. It is also being investigated for acute promyelocytic leukemia, relapsed mixed phenotype acute leukemia, and relapsed myelodysplastic syndrome.

The binding affinity of Uproleselan sodium to E-selectin is assessed using Surface Plasmon Resonance (SPR) technology. A typical SPR assay protocol is as follows: Recombinant human E-selectin protein is immobilized on a CM5 chip surface. Increasing concentrations of Uproleselan (0.1 nM–100 µM) are prepared in HBS-EP+ buffer (10 mM HEPES pH 7.4, 150 mM NaCl, 3 mM EDTA, 0.05% Tween-20) and flowed over the chip surface at 30 µL/min, with a 2-3 minute association phase and a 5-10 minute dissociation phase. SPR signal responses are monitored using a Biacore instrument, and data are fitted using a 1:1 Langmuir binding model to calculate the equilibrium dissociation constant KD. This assay gives a KD of approximately 0.46 µM for Uproleselan binding to human E-selectin . Functional blocking activity can be assessed by competition ELISA: E-selectin-Fc fusion protein is coated onto 96-well plates, biotin-labeled sialyl Lewisˣ and increasing concentrations of Uproleselan are added, and bound ligand is detected using streptavidin-HRP, yielding an IC50 of approximately 1.75 µM .
In vitro enzyme/receptor binding (non-cell) assays for Uproleselan involve measuring its binding affinity to E-selectin. Surface plasmon resonance (SPR) or ELISA-based binding assays are performed using recombinant E-selectin protein and varying concentrations of Uproleselan. Binding affinity (Kd = 0.46 µM) is determined from binding curves. Selectivity profiling against other selectins (e.g., P-selectin, L-selectin) is performed to confirm specificity.

In vitro cellular activity of Uproleselan sodium is primarily assessed by evaluating its blocking effect on leukemia cell adhesion to E-selectin and its enhancement of chemosensitivity. A typical assay protocol is as follows: CHO cells stably expressing human E-selectin or TNF-α-activated human umbilical vein endothelial cells (HUVECs) are cultured in medium containing 10% fetal bovine serum. Endothelial cells are seeded in 96-well plates (2×10⁴ cells per well) and cultured to confluence. Fluorescently labeled AML cell lines (such as KG-1a, OCI-AML3, 1×10⁵ cells per well) are added along with increasing concentrations of Uproleselan (0.1 nM–10 µM), and incubated at 37°C for 30-60 minutes. After gentle washing to remove non-adherent cells, adherent cells are quantified using a fluorescence plate reader to calculate IC50 values. Uproleselan at concentrations as low as 100 ng/mL inhibits >90% of KG-1a cell adhesion to recombinant E-selectin. Chemosensitization assays are performed under E-selectin-coated conditions: AML cells are treated with cytarabine (0.1-10 µM) and Uproleselan (5-20 µM) for 48-72 hours, and apoptosis rates are assessed by Annexin V/PI double staining flow cytometry or cell viability by MTS/CCK-8 assay.
In vitro cell-based experiments for Uproleselan are conducted using E-selectin-expressing endothelial cells and leukemic cell lines. Adhesion assays are performed where leukemic cells are allowed to adhere to E-selectin-coated surfaces or E-selectin-expressing endothelial cells in the presence of varying concentrations of Uproleselan. The compound's ability to block adhesion (IC50 = 1.75 µM) is quantified. Effects on leukemic cell survival, proliferation, and chemosensitivity are assessed.

In all study phases, uproleselan was administered as a 20-minute IV infusion given 24 hours prior, twice daily throughout, and twice daily for 48 hours postinduction chemotherapy. The salvage chemotherapy regimen used for patients with R/R disease was MEC (10 mg/m2 of mitoxantrone per day IV over 15-20 minutes, 100 mg/m2 of etoposide per day IV over 60 minutes, and 1000 mg/m2 of cytarabine per day IV over 60 minutes for 5 days) for 1 induction cycle. Uproleselan dose levels were determined by targeting a range of expected exposures, at or above the pharmacologically active dose range, as demonstrated in preclinical models. Based on available PK data from nonhuman primate studies and safety data from human volunteer studies, the starting dose for uproleselan administered with MEC in the dose-escalation phase of the study was 5 mg/kg. Uproleselan was administered across 3 pharmacologically active dose levels (5, 10, and 20 mg/kg). Dose escalation was performed in the absence of dose-limiting toxicity (DLT), defined as myelosuppression (failure of recovery to absolute neutrophil count [ANC] ≥0.5 × 109/L and platelet count of ≥25 × 109/L) beyond day 42 in the absence of persistent morphologic evidence of leukemia in the marrow or grade 3 nonhematologic toxicity attributable to uproleselan and not resolving to grade 2 by day 42. The dose-escalation committee determined an RP2D of 10 mg/kg, defined as the dose that (1) did not cause DLT in >33% of treated patients during induction and (2) was the most appropriate dose for continuing clinical evaluation in AML based on available data (safety, exposure achieved, pharmacodynamic [PD] assessment of on-target effect, clinical activity, and overall toxicity).[1]
The phase 2 dose expansion at the RP2D continued enrolling patients with R/R AML. Responding patients were eligible to receive 1 additional cycle of consolidation with uproleselan combined with a 4-day course of MEC. Alternatively, patients underwent hematopoietic stem cell transplantation and/or received additional postremission therapies at the discretion of their treating physician.[1]
A second cohort of newly diagnosed patients age ≥60 years were enrolled between June 2016 and February 2017 and treated with uproleselan administered at the RP2D in combination with conventional 7 + 3 induction chemotherapy (200 mg/m2 of cytarabine by a 24-hour continuous daily infusion on days 1-7 in combination with 12 mg/m2 of idarubicin by IV bolus daily on days 1-3). Uproleselan was administered on the same schedule as that used in the R/R AML cohort. For patients with residual leukemia detected on a day-15 midcycle bone marrow examination, a second cycle of induction therapy (5 + 2) was allowed in combination with uproleselan at the same dose and schedule as those used during the initial 7 + 3 induction. The first 3 patients were assessed postinduction for DLT; thereafter, enrollment was opened to complete a 25-patient cohort. Responders could receive consolidation therapy with uproleselan plus intermediate-dose cytarabine (2000 mg/m2 per day over 3 hours for 5 days or 1500 mg/m2 over 3 hours every 12 hours on days 1, 3, and 5) for up to 3 cycles. Patients could undergo hematopoietic stem cell transplantation at the discretion of their treating physician.[1]

---

Safety assessments[1]
The primary end point of the study was the frequency, severity, and relatedness of treatment-emergent adverse events (TEAEs) in patients receiving uproleselan in combination with chemotherapy. Safety assessments included the surveillance and recording of TEAEs, vital sign measurements, clinical laboratory tests, ECOG performance status, and physical examinations. Grade and term of TEAEs were reported by the treating physician and were graded by the Common Terminology Criteria for Adverse Events (version 4.03).

---

The in vivo efficacy of Uproleselan sodium is evaluated using various animal models. In AML mouse models, 8-12 week old female NSG or C57BL/6J mice are injected via the tail vein with MV4-11 or MLL-AF9 AML cells (1×10⁶-5×10⁶ per mouse). After leukemia establishment, mice are randomized into groups: vehicle control group, chemotherapy group (cytarabine 100 mg/kg, intraperitoneal injection, days 1-5), Uproleselan monotherapy group (25-50 mg/kg, intraperitoneal injection, once or twice daily), and combination therapy group. Leukemia burden is monitored by bioluminescence imaging, and survival curves are recorded to assess overall survival . In an HSCT transplantation model, C57BL/6J mice receive lethal irradiation (6 Gy × 2), and 24 hours later are injected intravenously with 1×10⁶ congenic donor bone marrow cells, with Uproleselan (40 mg/kg, intraperitoneal injection) administered according to various regimens (twice daily on days 0-1, days 1-2, or day 1 only), and 30-day survival is monitored . Additionally, in chemosensitization studies, Uproleselan combined with daunorubicin and cytarabine shows significant activity in multiple AML mouse models .
In vivo animal experiments for Uproleselan are performed in xenograft mouse models of AML and other hematological malignancies. Uproleselan is administered intravenously in combination with chemotherapy. Tumor growth, leukemic cell burden in bone marrow and peripheral blood, and survival are assessed. The compound's ability to enhance chemotherapy efficacy and reduce toxicity is evaluated. Clinical trials in humans have also been conducted.

The pharmacokinetic profile of Uproleselan sodium has been characterized through multiple clinical studies. In Phase I/II clinical trials, intravenously administered Uproleselan exhibits favorable pharmacokinetic characteristics. Doses ranging from 5-20 mg/kg were evaluated in relapsed/refractory AML patients, and the recommended Phase II dose (RP2D) was established as 10 mg/kg administered intravenously twice daily . An ongoing Phase I study in Chinese patients (CTR20202196/NCT04839341) is evaluating the pharmacokinetic profile of Uproleselan combined with chemotherapy in Chinese relapsed/refractory AML patients, including parameters such as Cmax, Tmax, AUC₀-₁₂, and AUC₀₋ₜ . Studies in healthy volunteers show that Uproleselan has an elimination half-life (t₁/₂) of several hours and distributes primarily in blood and extracellular spaces. Functional E-selectin blockade is achieved at a plasma concentration of approximately 38 µM in patients .
Uproleselan sodium is administered intravenously. The compound is a glycomimetic small molecule (MW 1326.49) with suitable properties for intravenous administration. Detailed pharmacokinetic parameters, including half-life, clearance, and volume of distribution, are available from clinical studies.

Dose escalation cohort [1]
In the dose escalation phase, a total of 19 patients were enrolled and divided into three different uproleselan dose groups: 5 mg/kg (n = 6), 10 mg/kg (n = 7), and 20 mg/kg (n = 6). Uproleselan at 10 mg/kg twice daily was identified as RP2D and was used in combination with MEC in the dose expansion phase, as well as in combination with idarubicin and cytarabine in the newly diagnosed cohort. No dose-limiting toxicities (DLTs) were observed in any of the dose groups in the phase 1 trial; therefore, DLTs did not affect the dose selection in the phase 2 trial. Pharmacodynamic (PD) analysis showed that the release of soluble E-selectin in plasma was reduced in all three dose groups, indicating that the drug had targeting activity. In addition, no dose response was observed, suggesting that the three dose groups evaluated may have exceeded the plateau of PD effects. Clinical outcomes (bone marrow response to proroleselan in combination with MEC-induced chemotherapy) were similar across the dose groups. Based on the pharmacokinetic analysis of the Phase I portion of this study, the 10 mg/kg procelandine dose group provided the highest level of drug exposure without exceeding the 14-day non-clinical safety limit, and therefore this dose was selected for further testing in the Phase II portion.

---

Relapsed/Refractory Acute Myeloid Leukemia (R/R AML) Cohort [1]
For all R/R AML patients, regardless of whether it was related to the study drug, the incidence of adverse events (TEAEs) during treatment was similar across all procelandine dose groups (Supplementary Table 1). None of the 66 R/R AML patients discontinued treatment due to adverse events. As expected, all patients in this R/R cohort experienced Grade 4 myelosuppression (thrombocytopenia, neutropenia, or anemia) during the study period. For patients achieving remission (complete remission [CR] or complete remission with incomplete recovery of blood cell counts [CRi]), the median time to recovery of blood cell counts (absolute neutrophil count ≥500/μL and platelet count ≥50/μL) was 33.0 days (90% CI, 31.0–34.0). Table 2 shows the overall incidence of grade 3 or 4 treatment-interventional adverse events (TEAEs). Most observed TEAEs were typical adverse events of background chemotherapy, with only a few TEAEs attributed to uproleselan (Supplementary Table 2 provides an overview of TEAEs by dose). Apart from hematologic toxicities, the only grade 3 or 4 TEAE with an incidence ≥10% was sepsis (12% of patients). Gastrointestinal toxicities, including nausea, vomiting, diarrhea, and colitis, were all mild, with an incidence of grade 3 adverse events <5%. Most treatment-emergent adverse events (TEAEs) occurring during liver and kidney treatment were Grade 1 or 2, with Grade 3 or 4 events occurring in 5% and 5% of patients, respectively. One patient (2%) died within 30 days of treatment initiation; the 60-day mortality rate was 9% (n = 6). Grade 3 mucositis was reported in only 2% of patients. Other non-hematologic adverse events were mild and generally considered unrelated to uproleselan.

---

Uproleselan sodium has demonstrated a favorable safety and tolerability profile in both preclinical and clinical studies. In Phase I/II clinical trials (n=19 initial patients), no dose-limiting toxicities (DLTs) were observed when Uproleselan was combined with MEC chemotherapy, leading to the selection of 10 mg/kg intravenous twice daily as the recommended Phase II dose . In relapsed/refractory AML patients (n=47 at RP2D), the most common grade 3/4 treatment-emergent adverse events were associated with chemotherapy itself rather than Uproleselan. Notably, Uproleselan combined with chemotherapy was associated with very low rates of oral mucositis, with severe mucositis observed in only 2% of relapsed/refractory patients . This finding is consistent with preclinical observations that Uproleselan protects against chemotherapy-induced mucositis by reducing inflammatory macrophage infiltration in the intestine . Preclinical studies show that Uproleselan reduces bone marrow toxicity including neutropenia, protects and increases the percentage of HSCs, enhances neutrophilic recovery, and reduces small intestine mucositis . In an HSCT mouse model, no signs of hepatic veno-occlusive disease were observed in Uproleselan-treated groups, and all surviving mice showed evidence of successful hematopoietic reconstitution . A Phase I study in Chinese R/R AML patients is ongoing to further evaluate safety and tolerability .
Preclinical and clinical toxicology studies have been conducted to evaluate the safety profile of Uproleselan. The compound is generally well-tolerated at therapeutic doses. Clinical trials have evaluated the safety and efficacy of Uproleselan in combination with chemotherapy in AML patients. The safety profile supports its continued development for hematological malignancies.

[1]. Phase 1/2 study of uproleselan added to chemotherapy in patients with relapsed or refractory acute myeloid leukemia. Blood. 2021 Sep 20;blood.2021010721.

In summary, the results of this phase 1/2 clinical trial support the biological and clinical rationale for targeting E-selectin and support the development of a confirmatory randomized controlled trial to further evaluate the benefits of adding uproleselan to salvage chemotherapy regimens in patients with relapsed/refractory disease and to anthracycline therapy regimens in elderly patients with AML. Randomized trials in these two populations are currently underway. [1]
Uproleselan sodium is also known as GMI-1271 and GGI-1271. It is a small molecule E-selectin antagonist originally targeted at AML as an adjuvant to standard chemotherapy for hematological malignancies. The compound has completed Phase II clinical trials, with Phase III studies ongoing. Its unique mechanism of action—disrupting E-selectin-mediated leukemic cell adhesion to the bone marrow niche—makes it a promising agent for improving outcomes in AML and other hematological malignancies.

C60H108N3NAO28

1342.5068

1325.706

1914993-95-5

1914993-95-5 (sodium); 1983970-12-2 (free acid)

129900385

Typically exists as solid at room temperature

8

27

52

91

1870

15

[Na+].O([C@H]1[C@@H]([C@H]([C@H]([C@@H](CO)O1)O)O[C@H](C(=O)[O-])CC1CCCCC1)NC(C)=O)[C@@H]1C[C@H](C(NCCNC(CCOCCOCCOCCOCCOCCOCCOCCOCCOCCOCCOCCOC)=O)=O)C[C@H](CC)[C@H]1O[C@H]1[C@H]([C@@H]([C@@H]([C@H](C)O1)O)O)O

WGEPSMSKGCZVTP-BPLQDBDISA-M

InChI=1S/C60H109N3O28.Na/c1-4-43-37-44(38-45(55(43)91-60-54(71)53(70)51(68)47(39-64)90-60)88-59-50(63-41(2)66)56(52(69)48(40-65)89-59)87-46(58(73)74)36-42-8-6-5-7-9-42)57(72)62-12-11-61-49(67)10-13-76-16-17-78-20-21-80-24-25-82-28-29-84-32-33-86-35-34-85-31-30-83-27-26-81-23-22-79-19-18-77-15-14-75-3/h42-48,50-56,59-60,64-65,68-71H,4-40H2,1-3H3,(H,61,67)(H,62,72)(H,63,66)(H,73,74)/q+1/p-1/t43-,44+,45+,46-,47-,48+,50+,51+,52-,53+,54-,55+,56+,59+,60-/m0./s1

Sodium (2S)-2-(((2R,3R,4R,5R,6R)-3-acetamido-2-(((1R,2R,3S,5R)-5-((2-(4,7,10,13,16,19,22,25,28,31,34,37-dodecaoxaoctatriacontanamido)ethyl)carbamoyl)-3-ethyl-2-(alpha-L-galactopyranosyloxy)cyclohexyl)oxy)-5-hydroxy-6-(hydroxymethyl)oxan-4-yl)oxy)-3-cyclohexylpropanoate

GMI1271; GMI 1271; Uproleselan sodium; Uproleselan sodium [USAN]; 1914993-95-5; 17ZJN0Q4CJ; GMI-1271 SODIUM; ABI701; Uproleselan (sodium); E-selectin antagonist gmi-1271; GMI-1271

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.)