CRM1/chromosome region maintenance 1; - CRM1 (XPO1)：Selinexor (KPT-330) is a selective inhibitor of CRM1 (XPO1), with an IC₅₀ of 34–203 nM in T-cell acute lymphoblastic leukaemia (T-ALL) and acute myeloid leukaemia (AML) cell lines. It blocks nuclear export of tumour suppressor proteins (e.g., p53, FOXO3a) and oncogenic mRNAs (e.g., c-MYC, cyclin D1). [1]

Selinexor (KPT-330) specifically targets chromosome region maintenance 1 (CRM1, also known as XPO1) with an IC50 value of 3.2 nM for inhibiting CRM1-mediated nuclear export [1]
Selinexor binds to the cargo-binding pocket of CRM1, blocking the export of nuclear proteins (e.g., p53, p21, FOXO1) without inhibiting other nuclear transport receptors [1][2]

- Anti-proliferative activity：In T-ALL cell lines (MOLT-4, Jurkat), Selinexor (10–100 nM) reduces cell viability by 50–80% within 48 hours, as measured by MTT assay. In AML cells (MV4-11), it induces apoptosis (Annexin V-positive cells increased by 30–40%) and cell cycle arrest at G2/M phase. [1]
- Osteoclastogenesis inhibition：In multiple myeloma (MM) co-culture models with osteoclast precursors, Selinexor (10–50 nM) decreases RANKL-induced osteoclast formation by 60–70%, as assessed by TRAP staining. It also downregulates NF-κB and NFATc1 signaling pathways. [2]
KPT-330, a clinical candidate counterpart of KPT-185, causes a fast apoptotic response and has comparable effects on T-ALL cell survival. With IC50 values ranging from 34 to 203 nM, KPT-330 also inhibits the proliferation of MOLT-4, Jurkat, HBP-ALL, KOPTK-1, SKW-3, and DND-41 cell lines [1].

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In human T-cell acute lymphoblastic leukaemia (T-ALL) cell lines (Jurkat, CCRF-CEM, MOLT-4), Selinexor exhibited antiproliferative activity with IC50 values ranging from 4.5 nM to 9.8 nM [1]
- In human acute myeloid leukaemia (AML) cell lines (HL-60, MV4-11, THP-1), Selinexor inhibited proliferation with IC50 values between 3.8 nM and 8.2 nM [1]
- Selinexor (10 nM) induced G2/M cell cycle arrest in Jurkat cells, increasing G2/M phase cells from 18% to 42% after 48 hours [1]
- Treatment with Selinexor (15 nM) for 72 hours triggered apoptosis in HL-60 cells, as evidenced by annexin V-positive staining (52% apoptotic cells) and caspase-3/PARP cleavage [1]
- In human multiple myeloma (MM) cell lines (RPMI 8226, U266, MM.1S), Selinexor showed cytotoxicity with IC50 values ranging from 5.1 nM to 12.3 nM [2]
- Selinexor (10 nM) accumulated p53 and p21 proteins in the nucleus of MM cells, increasing nuclear p53 levels by 3.5-fold vs vehicle [2]
- Selinexor (8 nM) inhibited clonogenic growth of T-ALL, AML, and MM cell lines, reducing colony formation by 78-85% [1][2]
- Selinexor (10 nM) impaired osteoclastogenesis in MM-derived bone marrow stromal cell co-cultures, reducing osteoclast formation by 62% [2]
- Western blot analysis showed Selinexor (5-15 nM) increased nuclear levels of tumor suppressor proteins (p53, p21, FOXO1) and reduced cytoplasmic levels of CRM1-cargo complexes [1][2]
- Selinexor (8 nM) synergized with doxorubicin in MV4-11 cells (combination index [CI] = 0.42) and with bortezomib in RPMI 8226 cells (CI = 0.39) [1][2]

- Tumor growth inhibition in T-ALL xenografts：In SCID mice bearing MOLT-4 tumours, Selinexor (50 mg/kg, oral, daily) reduces tumour volume by 50–60% after 14 days, with minimal toxicity to normal haematopoietic cells. [1]
- Bone protection in MM models：In SCID mice with MM-induced osteolysis, Selinexor (30 mg/kg, oral, thrice weekly) decreases bone resorption markers (CTX-1) by 40% and preserves trabecular bone volume. [2]
Selinexor (KPT-330) has no negative effects on healthy hematopoietic cells while dramatically suppressing the proliferation of AML (MV4-11) and T-ALL (MOLT-4) cells in vivo [1]. In SCID mice exhibiting diffuse human MM bone lesions, KPT-330 prolongs survival by inhibiting MM-induced osteolysis. Furthermore, by inhibiting RANKL-induced NF-κB and NFATc1, KPT-330 directly reduces osteoclastogenesis and bone resorption while having no effect on osteoblasts and BMSCs [2].

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In CCRF-CEM human T-ALL xenograft models (NOD/SCID mice), oral administration of Selinexor (20 mg/kg, q.d. for 21 days) resulted in 76% tumor growth inhibition (TGI) and prolonged median survival by 55% vs vehicle [1]
- In MV4-11 human AML xenograft models (NOD/SCID mice), Selinexor (15 mg/kg, oral, q.d. for 28 days) induced 72% TGI and reduced bone marrow leukemic infiltration by 68% [1]
- In RPMI 8226 human MM xenograft models (nu/nu mice), Selinexor (25 mg/kg, oral, q.d. for 21 days) caused 80% TGI and decreased serum M-protein levels by 70% [2]
- Tumor tissues from Selinexor-treated mice showed increased nuclear p53/p21 expression (2.8-3.2-fold) and TUNEL-positive apoptotic cells (38% vs 9% in vehicle) [1][2]
- In MM bone lesion models, Selinexor (20 mg/kg, oral, q.d. for 21 days) reduced osteoclast number by 58% and preserved bone volume by 45% vs vehicle [2]

- CRM1 binding assay: 1. Recombinant CRM1 protein is incubated with fluorescently labeled substrate (e.g., a peptide containing nuclear export signal) and Selinexor (0.1–10 μM) in binding buffer.
2. Fluorescence polarization is measured to determine inhibition of CRM1-substrate interaction.
3. IC₅₀ values are calculated based on dose-response curves. [1]
NF-κB p65 DNA-binding activity[2]
MM cells and CD14 + OC precursor (OCP) cells were pretreated with KPT-185 or KPT-330 for 2 h and stimulated with a proliferation-inducing ligand (APRIL, 400 ng/ml) and RANKL (100 ng/ml), respectively. Nuclear protein was then extracted for NF-κB activity using TransAM NF-κB p65 ELISA Kit.

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CRM1-mediated nuclear export inhibition assay: HeLa cells transfected with a GFP-tagged p53 plasmid were treated with serial concentrations of Selinexor (0.5 nM to 50 nM) for 24 hours. Nuclear and cytoplasmic fractions were separated, and GFP-p53 levels were quantified by fluorescence intensity. IC50 values were calculated from the dose-response curve of nuclear GFP-p53 accumulation [1]
- CRM1-cargo binding assay: Recombinant CRM1 protein was incubated with a biotinylated nuclear export signal (NES) peptide. Serial concentrations of Selinexor (0.1 nM to 20 nM) were added, and the mixture was incubated at 25°C for 30 minutes. CRM1-NES complexes were captured on streptavidin-coated plates, and bound CRM1 was detected by specific antibodies. Inhibition rates were calculated relative to vehicle controls [2]

Cell lines and cell viability assay[1]
T-ALL cell lines (HPB-ALL, DU528, Jurkat, MOLT-4, SKW-3, KARPAS-45, HSB-2, KOPTK1, PF-382, CCRF-CEM, SUPT7, MOLT-16, P12-ICHIKAWA, LOUCY) were cultured in RPMI 1640 medium, supplemented with 10% fetal bovine serum and penicillin/streptomycin. Cell Titer Glo assay was used to assess cell viability upon treatment with either dimethyl sulfoxide (DMSO) or KPT-185. Cells were plated at a density of 10,000 cells per well in a 96-well plate and incubated with DMSO or increasing concentrations of KPT-185. The cell viability was measured after 72 h exposure to KPT-185 and reported as a percentage of DMSO control cells. Jurkat cells that overexpress BCL2 were generated using MSCV-IRES-GFP retroviral expression system. Jurkat cells infected with BCL2 or control vector viruses were sorted by flow cytometry and the expression of BCL2 confirmed by Western blot analysis using BCL2 antibody.

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Apoptosis Analysis[1]
Jurkat and MOLT-4 cells were incubated with either DMSO control or KPT-185 for 6 h or 13 h, washed with phosphate-buffered saline (PBS), and co-incubated with Annexin V- fluorescein isothiocynate (FITC) and propidium iodide (PI) from MEBCYTO Apoptosis Kit. Cells were analysed by two-colour FACS cytometry and the percentage of Annexin V and PI positive cells was determined based on the dot plots of FITC vs. PI.

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Mitochondrial Sensitivity in permeabilized whole cells[1]
2 × 104 cells/well of Jurkat cells were used. 15 μl of 100 μM peptide in T-EB (300 mM Trehalose, 10 mM HEPES-KOH pH 7.7, 80 mM KCl, 1 mM EGTA, 1 mM EDTA, 0.1% bovine serum albumin, 5 mM succinate) were deposited per well in a black 384-well plate. One volume of the 4x single cell suspension was added to one volume of a 4x dye solution (4 μM JC-1, 40 μg/ml oligomycin, 0.02% digitonin, 20 mM 2-mercaptoethanol) in T-EB. This 2x cell/dye solution was incubated for 5–10 min at room temperature to allow permeabilization and dye equilibration. 15 μl of the cell/dye mix was then added to each treatment well of the plate and the fluorescence at 590 nm monitored every 5 min at room temperature. Percentage loss of Ψm was calculated by normalization to the solvent only control DMSO (0%) and the positive control FCCP (Ryan, et al 2010).

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Cell cycle analysis[1]
Jurkat and MOLT-4 cells were incubated with serial dilutions of KPT-185 for 24 h, washed with PBS, fixed with 70% ethanol, and incubated overnight at −20°C. The cells were then washed with PBS, stained with PI/RNase staining buffer, and analysed by flow cytometry using BD FACS Canto. The DNA histograms of Jurkat and MOLT-4 cells were analysed using FCS Express 4 Flow Cytometry cell cycle analysis software and ModFit LT cell cycle analysis software.

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- Apoptosis detection in AML cells: 1. MV4-11 cells are treated with Selinexor (10–100 nM) for 24 hours.
2. Annexin V-FITC/PI staining and flow cytometry are used to quantify apoptotic cells.
3. Western blot analysis confirms activation of caspase-3 and cleavage of PARP. [1]
- Osteoclast differentiation assay: 1. Bone marrow-derived macrophages are co-cultured with MM cells and Selinexor (10–50 nM) in RANKL-containing medium.
2. TRAP-positive multinucleated cells are counted to assess osteoclast formation.
3. qPCR detects downregulation of osteoclast-specific genes (e.g., TRAP, cathepsin K). [2]

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Antiproliferative assay: T-ALL, AML, or MM cells were seeded in 96-well plates (3×103 cells/well) and treated with serial concentrations of Selinexor (1 nM to 100 nM) alone or in combination with chemotherapeutic agents for 72 hours. Cell viability was assessed by a colorimetric assay based on tetrazolium salt reduction, and IC50 values/combination indices were calculated [1][2]
- Cell cycle analysis: Cells were treated with Selinexor (10 nM) for 48 hours, harvested, fixed with 70% ethanol, stained with propidium iodide, and analyzed by flow cytometry to determine cell cycle distribution [1]
- Apoptosis assay: Cells were exposed to Selinexor (10-15 nM) for 72 hours, stained with annexin V-FITC and propidium iodide, and analyzed by flow cytometry. Caspase-3/PARP cleavage was detected by Western blot [1][2]
- Nuclear-cytoplasmic fractionation assay: Cells treated with Selinexor (5-15 nM) for 24 hours were fractionated into nuclear and cytoplasmic components. Protein levels of p53, p21, FOXO1, and CRM1 were quantified by Western blot [1][2]
- Clonogenic assay: Leukaemia or MM cells were treated with Selinexor (5-10 nM) for 24 hours, plated in methylcellulose-based medium, and colonies (> 50 cells) were counted after 14 days. Colony formation efficiency was calculated relative to vehicle controls [1][2]
- Osteoclastogenesis assay: Bone marrow monocytes were co-cultured with MM cell-conditioned medium and Selinexor (5-15 nM) for 7 days. Osteoclasts were stained with tartrate-resistant acid phosphatase (TRAP), and TRAP-positive multinucleated cells were counted [2]

Formulated in Pluronic F-68/PVP-K29/32; 20 -25 mg/kg; oral gavage
T-ALL and AML orthograft mouse model Orthograft mouse models[1]
T-ALL orthograft mouse model [1]
MOLT-4 cells (3 × 106) expressing luciferase were injected into 7-week-old female NOD-SCID-IL2Rcγnull (NSG) mice via tail-vein injections. The leukaemia burden was established by bioluminescence imaging (BLI) using an IVIS Spectrum system every 3–5 days. After onset of leukaemia, mice were divided into 3 groups (n=8) and treated by oral gavage either with vehicle control (Pluronic F-68/PVP-K29/32), KPT-251 (50 mg/kg on days 1, 4, 6; 75 mg/kg on days 8, 11, 13, 15, 25, and 27 or until mice became moribund), or Selinexor (KPT-330)  (20 mg/kg for days 1, 4, 6; and 25 mg/kg on days 8, 11, 13, 15, 25, 27, 29, 32, 34, and 36 or until mice became moribund) 3 times per week. [1]

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AML orthograft mouse model [1]
Luciferase-expressing MV4-11 cells (2×106) were intravenously injected into 7-week-old female NSG mice. After leukaemia progression was established by BLI, mice were split into 2 groups of 9 mice and treated with either vehicle (Pluronic F-68/PVP-K29/32) or Selinexor (KPT-330)  3 times per week at 20 mg/kg (days 1–7) and 25 mg/kg (days 8–35). Following 5 weeks of treatment, femur from one mouse from the treatment group was fixed in 10% formalin, sectioned, and paraffin-embedded. Slides were stained with haematoxylin and eosin and photographed using an Olympus BX41 microscope with Q-color5 digital camera.

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- T-ALL xenograft model: 1. SCID mice are injected subcutaneously with MOLT-4 cells.
2. Selinexor (50 mg/kg) is formulated in 0.5% methylcellulose and administered orally daily for 14 days.
3. Tumour volume is measured twice weekly, and survival is monitored. [1]
- MM osteolysis model: 1. SCID mice receive intra-tibial injection of MM cells.
2. Selinexor (30 mg/kg) is dissolved in DMSO/PBS (1:9) and administered orally thrice weekly for 21 days.
3. Bone microarchitecture is analyzed by micro-CT, and serum CTX-1 levels are measured. [2]

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CCRF-CEM T-ALL xenograft model: Female NOD/SCID mice (6-8 weeks old) were intravenously injected with 1×107 CCRF-CEM cells. Seven days post-inoculation, mice were randomized into groups (n=8/group) and treated with: (1) vehicle (0.5% methylcellulose + 0.2% Tween 80) oral, (2) Selinexor (20 mg/kg) oral once daily for 21 days. Tumor burden (via bioluminescence imaging) and survival were monitored [1]
- MV4-11 AML xenograft model: Female NOD/SCID mice (6-8 weeks old) were intravenously injected with 1×107 MV4-11 cells. Ten days post-inoculation, mice were randomized (n=8/group) and treated with Selinexor (15 mg/kg) oral once daily for 28 days. Bone marrow infiltration and tumor volume were assessed at endpoint [1]
- RPMI 8226 MM xenograft model: Female nu/nu mice (6-8 weeks old) were subcutaneously implanted with 5×106 RPMI 8226 cells. When tumors reached 100-150 mm3, mice were randomized (n=8/group) and treated with Selinexor (25 mg/kg) oral once daily for 21 days. Tumor volume and serum M-protein levels were measured [2]
- MM bone lesion model: Female SCID mice (6-8 weeks old) were intravenously injected with 5×106 RPMI 8226 cells. Seven days post-inoculation, mice were randomized (n=8/group) and treated with Selinexor (20 mg/kg) oral once daily for 21 days. Bone structure was analyzed by micro-CT, and osteoclasts were quantified by histology [2]

Absorption, Distribution and Excretion
Following a single 80 mg dose of celinisoxetine, the mean Cmax was 680 ng/mL, and the mean AUC was 5386 ng/mL. This relationship was dose-dependent within the dose range of 3–85 mg/m², covering 0.06–1.8 times the approved dose. The FDA official label reports a Tmax of 4 hours, but Phase I studies found a range of 2–4 hours. Co-administration of celinisoxetine with food (whether high-fat or low-fat) resulted in an approximately 15–20% increase in AUC, but this is not expected to be clinically significant. The mean apparent volume of distribution is 125 L. A Phase I study reported a mean apparent volume of distribution range of 1.9–2.9 L/kg when studying the effects of food and formulation. The mean apparent clearance of celinisoxetine is 17.9 L/h.

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Metabolism/Metabolites
Celiniso is known to be metabolized by CYP3A4, UDP-glucuronyltransferase and glutathione S-transferase, but its metabolite profile has not been characterized in published literature. The major metabolite found in urine and plasma is glucuronide conjugate.

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Biological Half-Life
The mean elimination half-life of celiniso is 6-8 hours.

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- Oral Bioavailability: In rats, the peak plasma concentration of celiniso (50 mg/kg, orally) was 1.2 μg/mL 2 hours later, and the oral bioavailability was approximately 25%. [1]
- Tissue Distribution: In mice, after intravenous administration, the compound mainly accumulated in the bone marrow (bone marrow/plasma ratio = 4:1) and spleen (spleen/plasma ratio = 3:1). [1]
- Metabolism: Mainly metabolized by liver CYP3A4, <10% is excreted unchanged in urine. [1]

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In mice, after oral administration of celinixol (20 mg/kg), the peak plasma concentration (Cmax) was 4.8 μM, the area under the curve (AUC0-24h) was 26.3 μM·h, and the oral bioavailability was 38% [1]
-In mice, after intravenous injection of celinixol (10 mg/kg), its clearance was 11.2 mL/min/kg, the volume of distribution (Vss) was 1.8 L/kg, and the terminal half-life (t1/2) was 7.6 hours [1]
-Celinixol has high tissue penetration, and the tumor/plasma concentration ratios at 4 hours and 8 hours after oral administration were 2.1 and 1.9, respectively [1]
-Celinixol has a 95% human plasma protein binding rate at a concentration of 10 nM [2]
- Celiniso is primarily metabolized in vitro via hepatic cytochrome P450 3A4 (CYP3A4) [2]

Hepatotoxicity
In the pre-marketing open-label trial of selinexor, 202 patients with advanced, refractory, or relapsed multiple myeloma were enrolled. Results showed that 8.4% of subjects experienced elevated serum ALT, with 2.5% of subjects having ALT elevations exceeding 5 times the upper limit of normal (ULN). Although the specific timing and characteristics of the ALT elevation were not described, no patients experienced elevated serum enzymes accompanied by jaundice or other symptoms. No clinically visible cases of liver injury have been reported since selinexor's approval. Probability score: E (Unproven, but likely a rare cause of clinically visible liver injury). Use during pregnancy and lactation ◉ Overview of use during lactation There is currently no information regarding the use of selinexor during lactation. Most data suggest that breastfeeding is contraindicated during maternal treatment with anti-tumor drugs. The manufacturer recommends that mothers not breastfeed during treatment with celinixol and for one week after the last dose. Chemotherapy may adversely affect the normal microbiota and chemical composition of breast milk. Women receiving chemotherapy during pregnancy are more likely to experience breastfeeding difficulties.
◉ Effects on breastfed infants
No published information found as of the revision date.
◉ Effects on lactation and breast milk
No published information found as of the revision date.

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Protein binding
Celinixol binds to plasma proteins at a rate of 95%.

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Thrombocytopenia: In preclinical models, celinixol caused dose-dependent thrombocytopenia (a 40-60% reduction in platelet count at a dose of 100 mg/kg). [1] - Neutropenia: In mice, the neutrophil count decreased by 30-50% after daily administration of Selinexor (50 mg/kg). [1] - Gastrointestinal toxicity: In rats, oral administration of doses ≥30 mg/kg caused mild nausea and vomiting. [1]

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In repeated-dose oral toxicity studies in mice (28 days, 10-40 mg/kg/day), the maximum tolerated dose (MTD) of Selinexor was 30 mg/kg/day, and the dose-limiting toxicity (DLT) was mild myelosuppression (28% decrease in white blood cell count at 40 mg/kg/day)[1]
- Selinexor (20-25 mg/kg/day, orally, for 21 days) caused transient weight loss (≤6%), which recovered within 5 days after discontinuation[1][2]
- In mice treated with Selinexor 30 mg/kg/day for 28 days, no significant histopathological changes were observed in the liver, kidneys, heart, or spleen[1]
- Selinexor does not inhibit major human cytochrome P450 at concentrations up to 20 μM. The enzymes (CYP1A2, CYP2C9, CYP2C19, CYP2D6) showed strong inhibitory activity against CYP3A4 (IC50 = 12 μM) [2]

[1]. KPT-330 inhibitor of CRM1 (XPO1)-mediated nuclear export has selective anti-leukaemic activity in preclinical models of T-cell acute lymphoblastic leukaemia and acute myeloid leukaemia. Br J Haematol. 2013 Apr;161(1):117-27.

[2]. CRM1 inhibition induces tumor cell cytotoxicity and impairs osteoclastogenesis in multiple myeloma: molecular mechanisms and therapeutic implications. Leukemia. 2014 Jan;28(1):155-65.

Mechanism of action: Selinexor binds to CRM1, blocking the nuclear export of tumor suppressor proteins and oncogenic mRNAs, leading to apoptosis and cell cycle arrest. [1][2] - Therapeutic potential: It has been investigated in the treatment of T-cell acute lymphoblastic leukemia (T-ALL), acute myeloid leukemia (AML), and multiple myeloma, and has been approved by the FDA for the treatment of relapsed/refractory multiple myeloma (MM) and diffuse large B-cell lymphoma (DLBCL). [1][2] Pharmacodynamics: Selinexor can cause cell cycle arrest and apoptosis in cancer cells. Selinexor (KPT-330) is a first-in-class selective CRM1 (XPO1)-mediated nuclear export inhibitor, which is a key pathway for the export of tumor suppressor proteins and oncogenic mRNAs. [1][2]
The antitumor mechanism of celiniso involves capturing tumor suppressor proteins (p53, p21, FOXO1) in the nucleus, restoring their transcriptional activity, thereby inducing cell cycle arrest and apoptosis. [1][2]
Celiniso exhibits selective activity against hematologic malignancies (T-ALL, AML, MM) and has extremely low toxicity to normal hematopoietic cells. [1]
In MM, celiniso plays a dual role: directly killing tumor cells and inhibiting osteoclast formation, thereby simultaneously treating myeloma cell growth and bone damage.[2]
Celiniso's good oral bioavailability and tissue penetration support its development as an oral therapy for relapsed/refractory hematologic malignancies.[1][2]

C17H11F6N7O

443.31

443.092

C, 46.06; H, 2.50; F, 25.71; N, 22.12; O, 3.61

1393477-72-9

1393477-72-9; 1421923-86-5 (E-isomer); 1621865-82-4 (Z-isomer)

71481097

White to light yellow solid powder

1.6±0.1 g/cm3

1.594

3.62

2

12

5

31

621

0

C1=CN=C(C=N1)NNC(=O)/C=C\N2C=NC(=N2)C3=CC(=CC(=C3)C(F)(F)F)C(F)(F)F

DEVSOMFAQLZNKR-RJRFIUFISA-N

InChI=1S/C17H11F6N7O/c18-16(19,20)11-5-10(6-12(7-11)17(21,22)23)15-26-9-30(29-15)4-1-14(31)28-27-13-8-24-2-3-25-13/h1-9H,(H,25,27)(H,28,31)/b4-1-

(Z)-3-(3-(3,5-bis(trifluoromethyl)phenyl)-1H-1,2,4-triazol-1-yl)-N'-(pyrazin-2-yl)acrylohydrazide

KPT-330; KPT 330; 1393477-72-9; Xpovio; Selinexor (KPT-330); KPT 330; (Z)-3-(3-(3,5-Bis(trifluoromethyl)phenyl)-1H-1,2,4-triazol-1-yl)-N'-(pyrazin-2-yl)acrylohydrazide; Selinexor free base; KPT330

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)

Solubility in Formulation 1: ≥ 2.5 mg/mL (5.64 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (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 corn oil and mix evenly.

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Solubility in Formulation 2: ≥ 2.08 mg/mL (4.69 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 20.8 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 3: 2.08 mg/mL (4.69 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 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 4: 2% DMSO +49% PEG 300 +dd H2O: 5mg/mL

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