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Fig. 1 · Structure
Cat. No.
A10906
CAS No.
162635-04-3
Formula
C56H87NO16
Mol. Weight
1030.3

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Temsirolimus

mTOR inhibitor

Temsirolimus is a specific inhibitor of mTOR and interferes with the synthesis of proteins that regulate proliferation, growth, and survival of tumor cells.

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Biological Activity

Target & Activity

Target Activity Value
mTOR (Cell-free assay) 1.76 μM

Cellular Effect

Cell Line Activity Value Description Reference
A498 IC50 0.35 μM Cytotoxicity against human A498 cells after 72 hrs by MTT assay [PMID: 25124114]
A498 IC50 0.5 μM Cytotoxicity against human A498 cells assessed as inhibition of cell viability after 6 days by MTT assay [PMID: 23360104]
A498 IC50 34.3 μM Cytotoxicity against human A498 cells after 72 hrs by MTT assay [PMID: 23489626]
A549 IC50 11.81 μM Antiproliferative activity against human A549 cells assessed as reduction in cell viability incubated for 24 hrs by MTT assay [PMID: 33862514]
HEK293 IC50 1.76 μM Inhibition of FKBP12-independent human recombinant mTOR expressed in HEK293 cells using His6-S6K1 as a substrate by DELFIA assay [PMID: 21438579]
LNCaP IC50 0.0005 μM Antiproliferative activity against human LNCAP cells after 3 days by MTS assay [PMID: 21438579]
MDA-MB-231 IC50 17.57 μM Antiproliferative activity against human MDA-MB-231 cells assessed as reduction in cell viability incubated for 24 hrs by MTT assay [PMID: 33862514]
MDA-MB-468 IC50 0.008 μM Antiproliferative activity against human MDA468 cells after 3 days by MTS assay [PMID: 21438579]
MDA-MB-468 IC50 10.89 μM Antiproliferative activity against human MDA-MB-468 cells assessed as reduction in cell viability incubated for 24 hrs by MTT assay [PMID: 33862514]

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In Vitro Studies

Temsirolimus directly bound purified FSP1 protein in vitro in an isothermal titration calorimetry assay, with a dissociation constant around 5.28 μM. In GPX4-KO BEL-7404 cells treated for 24 h, Temsirolimus robustly decreased cell viability, with a median lethal dose of 0.72–0.89 μM. [1]

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

Temsirolimus binding to purified protein

Biochemical assay · purified FSP1 protein in vitro [1]

In an isothermal titration calorimetry assay, Temsirolimus at 25 μM was titrated into purified FSP1 protein in vitro. Temsirolimus directly bound the protein, with a dissociation constant around 5.28 μM.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
isothermal titration calorimetry assaydissociation constant around 5.28 μM[1]

Literature-Reported Treatment Conditions

Treatment concentration
25 μM
Exposure duration
150-sec intervals
Method
titrated with injections of compounds
Vehicle
a buffer containing 20 mM Tris–HCl (pH 7.5), 100 mM NaCl, and 1% DMSO
Methods and source locations

Compound reported in the paper: Temsirolimus

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

Results > Temsirolimus induces ferroptosis by directly inhibiting FSP1 activity (S40, S41); Methods and materials > Isothermal titration calorimetry (S99, S100)

isothermal titration calorimetry assay: isothermal titration calorimetry assay; comparator: everolimus — Results > Temsirolimus induces ferroptosis by directly inhibiting FSP1 activity (S40)

Reduced viability in GPX4-KO BEL-7404 cells

Cell-based study · GPX4-KO BEL-7404 cells [1]

GPX4-KO BEL-7404 cells were treated with Temsirolimus for 24 h. Treatment robustly decreased cell viability, with a median lethal dose of 0.72–0.89 μM.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
cell viabilityLD50 0.72–0.89 μM[1]

Literature-Reported Treatment Conditions

Exposure duration
24 h
Reported limits
Not stated in the sentences used: dose, route, vehicle, control.
Methods and source locations

Compound reported in the paper: Temsirolimus

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

Results > Screening of FDA-approved drugs identifies potent ferroptosis inducers in liver cancer cells (S20); Figure 2 legend (S143)

cell viability: cell viability — Results > Screening of FDA-approved drugs identifies potent ferroptosis inducers in liver cancer cells (S20); Figure 2 legend (S143)

In Vivo Studies

In NSG-HPRT null mice bearing a PDX model, daily intraperitoneal Temsirolimus treatment consistently abrogated tumor growth in a comparison with vehicle or carboplatin. Tumor growth resumed upon withdrawal of Temsirolimus. [2]

Temsirolimus treatment and withdrawal in a PDX model

Animal study · NSG-HPRT null mice; PDX model [2]

In NSG-HPRT null mice bearing a PDX model, daily intraperitoneal Temsirolimus treatment consistently abrogated tumor growth in a comparison with vehicle or carboplatin. Tumor growth resumed upon withdrawal of Temsirolimus.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Tumor growth was measured biweekly using calipersReported result Treatment with temsirolimus consistently demonstrated abrogation of tumor growth; upon withdrawal of temsirolimus treatment, there was a resumption of tumor growth in the PDX model.[2]

Conditions shared by the study groups

Route
intraperitoneally (IP)
Treatment course
daily
Vehicle
N-Methyl-2-pyrrolidone (NMP); PTD buffer (30 % PEG-400; 5 % Tween 80; 65 % Dextrose water, D5W, Sigma Aldrich)
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Temsirolimus 20 mg/kgvehicleTreatment with temsirolimus consistently demonstrated abrogation of tumor growth; upon withdrawal of temsirolimus treatment, there was a resumption of tumor growth in the PDX model.[2]
Temsirolimus 20 mg/kg
Model: NSG-HPRT null mice; PDX model
Methods and source locations

Compound reported in the paper: Temsirolimus

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

Methods > Chemical reagents (S3); Methods > Patient-derived xenograft (PDX) generation (S4, S7); Methods > PDX treatment studies (S9); Results > Preclinical assessment of therapeutic targeting of mTOR, MEK, and MYC pathways (S169, S173, S188)

Tumor growth was measured biweekly using calipers: Tumor growth was measured biweekly using calipers; comparator: vehicle — Methods > Patient-derived xenograft (PDX) generation (S7); Results > Preclinical assessment of therapeutic targeting of mTOR, MEK, and MYC pathways (S173, S188)

Temsirolimus 20 mg/kg · Methods > PDX treatment studies (S9); Results > Preclinical assessment of therapeutic targeting of mTOR, MEK, and MYC pathways (S173, S188)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 162635-04-3
Applications mTOR inhibitor
Formula C56H87NO16
Molecular Weight 1030.3
Synonyms CCI-779; Torisel
SMILES
C[C@@H]1CC[C@H]2C[C@@H](/C(=C/C=C\C=C\[C@H](C[C@H](C(=O)[C@H]([C@H](/C(=C\[C@H](C(=O)C[C@H](OC(=O)[C@@H]3CCCCN3C(=O)C(=O)[C@@]1(O2)O)[C@@H](C)C[C@@H]4CC[C@H]([C@@H](C4)OC)OC(=O)C(C)(CO)CO)C)/C)O)OC)C)C)/C)OC

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 60 mg/mL (58.24 mM)
Water Insoluble
Ethanol 67 mg/mL (65.03 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.

In Vivo Preparation

Concentration
6 mg/mL
Vehicle
2% DMSO+30% PEG 300 +2% Tween 80+ddH2O

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] Tian RL, Wang TX, Huang ZX, et al. Temsirolimus inhibits FSP1 enzyme activity to induce ferroptosis and restrain liver cancer progression. J Mol Cell Biol (2025). PMID: 39313331 DOI: 10.1093/jmcb/mjae036 Source material
  2. [2] Dela Cruz FS, Diolaiti D, Turk AT, et al. A case study of an integrative genomic and experimental therapeutic approach for rare tumors: identification of vulnerabilities in a pediatric poorly differentiated carcinoma. Genome Med (2016). PMID: 27799065 DOI: 10.1186/s13073-016-0366-0 Source material

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