Fig. 1 · Structure

Documents & Downloads

Ispinesib (SB-715992)

Cat. No. A10486 CAS 336113-53-2

KSP Inhibitor

Ispinesib (SB-715992) is a potent inhibitor of kinesin spindle protein, a kinesin motor protein essential for the formation of a bipolar mitotic spindle and cell cycle progression through mitosis.

In Stock

Free Aliquoting for Your Order

Tell us your preferred amount per vial. We’ll confirm the options.

Biological Activity

Target & Activity

Target Activity Value
KSP (HsEg5) (Cell-free assay) 1.7 nM(Ki app)

Cellular Effect

Cell Line Activity Value Description Reference
BXPC-3 GI50 80 nM Growth inhibition of human BxPC3 cells after 72 hrs by Alamar blue assay [PMID: 23394180]
BXPC-3 GI50 80 nM Antiproliferative activity against human BxPC3 cells after 72 hrs by Alamar blue assay [PMID: 22248262]
HCT-116 IC50 1.1 nM Growth inhibition of human HCT116 cells after 72 hrs by MTS assay [PMID: 26396688]
HCT-116 GI50 25 nM Growth inhibition of human HCT116 cells after 72 hrs by Alamar blue assay [PMID: 23394180]
HCT-116 GI50 25 nM Antiproliferative activity against human HCT116 cells after 72 hrs by Alamar blue assay [PMID: 22248262]
HeLa IC50 1 μM Antiproliferative activity against human HeLa cells after 48 hrs by MTT assay [PMID: 24184776]
K562 GI50 71 nM Antiproliferative activity against human K562 cells after 72 hrs by Alamar blue assay [PMID: 22248262]
LNCaP GI50 22 nM Growth inhibition of human LNCAP cells after 72 hrs by Alamar blue assay [PMID: 23394180]
MCF7 IC50 1.3 μM Antiproliferative activity against human MCF7 cells after 48 hrs by MTT assay [PMID: 24184776]
NCI-H1299 GI50 82 nM Growth inhibition of human NCI-H1299 cells after 72 hrs by Alamar blue assay [PMID: 23394180]
NCI-H1299 GI50 82 nM Antiproliferative activity against human NCI-H1299 cells after 72 hrs by Alamar blue assay [PMID: 22248262]
PC-3 GI50 50 nM Growth inhibition of human PC3 cells after 72 hrs by Alamar blue assay [PMID: 23394180]

12 records · Scroll to view more

In Vitro Studies

Human GBM surgical specimen slice cultures treated with 1.8 nM Ispinesib for 18 h showed depletion of a MES/AC signature and enrichment of cell cycle signatures, except in an outlier patient’s slice culture. In Panc1 cells, 10 nmol/L Ispinesib for 96 hours significantly increased multinucleation to 44.9%, compared with 4.1% in vehicle-treated cells. In TS543 cells, Ispinesib alone reached maximum efficacy at 25%–20% viability. [1,2]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Ispinesib and transcriptional signatures in human glioblastoma slices

Cell-based study · slice cultures from human GBM surgical specimens [1]

Human GBM surgical specimen slice cultures received 1.8 nM Ispinesib for 18 h. Treatment depleted a MES/AC signature and enriched cell cycle signatures, except in an outlier patient’s slice culture.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
scRNA-seqReported result 1.8 nM ispinesib; 18 h: depletion of a MES/AC signature and enrichment of cell cycle signatures in four patients’ slice cultures, consistent with the TS543 ispinesib-resistant phenotype, except for the outlier patient’s slice culture.[1]

Literature-Reported Treatment Conditions

Treatment concentration
1.8 nM
Exposure duration
18 h
Method
the medium was replaced with pre-warmed medium containing drugs
Vehicle
DMSO
Methods and source locations

Compound reported in the paper: Ispinesib

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

RESULTS > Ispinesib-treated GBM patient slice cultures share phenotypic features with TS543 ispinesib-resistant phenotype (S41, S44); STAR★METHODS > METHOD DETAILS > Human glioma patient ex vivo tissue slices acute drug treatment (S120, S122); Figure 3. legend (S183)

scRNA-seq: scRNA-seq; comparator: corresponding volume of vehicle (DMSO) — RESULTS > Ispinesib-treated GBM patient slice cultures share phenotypic features with TS543 ispinesib-resistant phenotype (S41, S44); STAR★METHODS > METHOD DETAILS > Human glioma patient ex vivo tissue slices acute drug treatment (S120, S122)

Ispinesib and multinucleation in pancreatic cancer cells

Cell-based study · Panc1 cells [2]

Panc1 cells received 10 nmol/L Ispinesib for 96 hours. The proportion of multinucleated cells increased significantly to 44.9%, compared with 4.1% in DMSO vehicle-treated cells.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
proportion of multinucleated cellsproportion of multinucleated cells 10 nmol/L ispinesib for 96 hours: 44.9%[2]

Literature-Reported Treatment Conditions

Treatment concentration
10 nmol/L
Exposure duration
96 hours
Vehicle
DMSO
Reported limits
Not stated in the sentences used: route.
Methods and source locations

Compound reported in the paper: Ispinesib

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

MATERIALS AND METHODS > Immunofluorescence staining (S46); FIGURE 2 legend (S180, S182, S183)

proportion of multinucleated cells: proportion of multinucleated cells; comparator: DMSO vehicle‐treated cells — MATERIALS AND METHODS > Immunofluorescence staining (S46); FIGURE 2 legend (S182)

Ispinesib efficacy in a cell viability assay

Cell-based study · TS543 cells [1]

TS543 cells were treated with Ispinesib, and viability was assessed using PrestoBlue Cell Viability Reagent. Ispinesib alone reached maximum efficacy of 25%–20% viability.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Cell viability was assessed with PrestoBlue Cell Viability Reagentcell viability 25%–20% viability[1]

Literature-Reported Treatment Conditions

Exposure duration
treated with inhibitor for three days
Reported limits
Not stated in the sentences used: dose, route, vehicle, control.
Methods and source locations

Compound reported in the paper: Ispinesib

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

RESULTS > Identification of synergistic drug targets from gene expression analysis of ispinesib-resistant clones in the drug-naive setting (S84); STAR★METHODS > METHOD DETAILS > Dose response assays (S129, S130)

Cell viability was assessed with PrestoBlue Cell Viability Reagent: Cell viability was assessed with PrestoBlue Cell Viability Reagent — RESULTS > Identification of synergistic drug targets from gene expression analysis of ispinesib-resistant clones in the drug-naive setting (S84); STAR★METHODS > METHOD DETAILS > Dose response assays (S130)

In Vivo Studies

Female NSG mice with intracranial GBM1A implants received intraperitoneal Ispinesib at 10 mg/kg. Ispinesib alone prolonged survival compared with vehicle, with a median survival of 74 days. [3]

Ispinesib and survival in an intracranial glioblastoma model

Animal study · Female NSG mice were intracranially implanted with 500,000 luciferase expressing GBM1A cells [3]

Female NSG mice with intracranial GBM1A implants received intraperitoneal Ispinesib at 10 mg/kg. Ispinesib alone prolonged survival compared with vehicle, with a median survival of 74 days.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Kaplan Meier survival curvesmedian survival 10 mg/kg ispinesib, once every 4 days for 28 days: median survival 74 days[3]

Conditions shared by the study groups

Route
ip
Treatment course
After 7 days, animals were randomized into four groups and ip administered with microemulsion vehicle, 10 mg/kg elacridar, 10 mg/kg ispinesib, or a combination of 10 mg/kg ispinesib and 10 mg/kg elacridar, once every 4 days for 28 days (n = 10).
Vehicle
microemulsion vehicle
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Ispinesib 10 mg/kgvehicletreatment with ispinesib alone prolongs survival compared to vehicle or elacridar (p < 0.0001, log rank test)[3]
Ispinesib 10 mg/kg
Model: Female NSG mice were intracranially implanted with 500,000 luciferase expressing GBM1A cells
Methods and source locations

Compound reported in the paper: Ispinesib

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Results > Elacridar significantly enhances the efficacy of systemically administered ispinesib in a rodent model of GBM (S99, S100, S101); Materials and Methods > In vivo efficacy of ispinesib in a mouse model of GBM (S141, S142)

Kaplan Meier survival curves: Kaplan Meier survival curves; comparator: vehicle — Results > Elacridar significantly enhances the efficacy of systemically administered ispinesib in a rodent model of GBM (S99, S100, S101); Materials and Methods > In vivo efficacy of ispinesib in a mouse model of GBM (S142)

Ispinesib 10 mg/kg · Results > Elacridar significantly enhances the efficacy of systemically administered ispinesib in a rodent model of GBM (S101); Materials and Methods > In vivo efficacy of ispinesib in a mouse model of GBM (S142)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 336113-53-2
Applications KSP Inhibitor
Formula C30H33ClN4O2
Molecular Weight 517.1
Synonyms Ispinesib mesylate; B-715992; CK 0238273; SB-715992
SMILES
CC1=CC=C(C=C1)C(=O)N(CCCN)[C@@H](C2=NC3=C(C=CC(=C3)Cl)C(=O)N2CC4=CC=CC=C4)C(C)C

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 93 mg/mL (179.86 mM)
Water Insoluble
Ethanol 93 mg/mL (179.86 mM)

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Cheng YL, Banu MA, Zhao W, et al. Multiplexed single-cell lineage tracing of mitotic kinesin inhibitor resistance in glioblastoma. Cell Rep (2024). PMID: 38652658 DOI: 10.1016/j.celrep.2024.114139 Source material
  2. [2] Murase Y, Ono H, Ogawa K, et al. Inhibitor library screening identifies ispinesib as a new potential chemotherapeutic agent for pancreatic cancers. Cancer Sci (2021). PMID: 34510663 DOI: 10.1111/cas.15134 Source material
  3. [3] Gampa G, Kenchappa RS, Mohammad AS, et al. Enhancing Brain Retention of a KIF11 Inhibitor Significantly Improves its Efficacy in a Mouse Model of Glioblastoma. Sci Rep (2020). PMID: 32300151 DOI: 10.1038/s41598-020-63494-7 Source material

Added to your cart

View Cart Checkout
Loading...