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Fig. 1 · Structure
Cat. No.
A10955
CAS No.
877877-35-5
Formula
C33H35NO6S
Mol. Weight
573.7

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TW-37

Cat. No. A10955 CAS 877877-35-5

Bcl-2 inhibitor

TW-37, a small-molecule inhibitor of Bcl-2, inhibits cell growth and induces apoptosis in pancreatic cancer mediated through a novel pathway involving inactivation of Notch-1 and Jagged-1.

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Biological Activity

Target & Activity

Target Activity Value
Mcl-1 (Cell-free assay) Ki 0.26 μM
Bcl-2 (Cell-free assay) Ki 0.29 μM
Bcl-xL (Cell-free assay) Ki 1.11 μM

In Vitro Studies

In SHED, treatment at 10 μM for 6 h was associated with secretory VEGF levels more than 2‐fold higher than in non‐treated cells. In HepG2-SR, treatment with the compound for 48 h, using control vehicle as the control, yielded a half-maximal inhibitory concentration of 43.477 µM. WSU-pre-B-ALL samples received the study compound at concentrations up to 750 nM for 72 hr, with untreated samples as controls. The concentration producing 50% growth inhibition was 180 nM. [1,2,3]

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

Increased VEGF Secretion in Treated SHED

Cell-based study · SHED [1]

In SHED, treatment at 10 μM for 6 h was associated with secretory VEGF levels more than 2‐fold higher than in non‐treated cells.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Secretory VEGF levelsVEGF secretion more than 2‐fold higher[1]

Literature-Reported Treatment Conditions

Treatment concentration
10 μM
Exposure duration
6 h
Reported limits
Not stated in the sentences used: route, vehicle.
Methods and source locations

Compound reported in the paper: TW-37

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

Results > TW‐37, ML228, and CPX, as Optimal HIF‐1α Stabilizers, Effectively Stabilized HIF‐1α in SHED and Promoted VEGF Secretion (S200); FIGURE 2 legend (S268)

Secretory VEGF levels: Secretory VEGF levels; comparator: non‐treated cells — Results > TW‐37, ML228, and CPX, as Optimal HIF‐1α Stabilizers, Effectively Stabilized HIF‐1α in SHED and Promoted VEGF Secretion (S200); FIGURE 2 legend (S268)

Compound Inhibitory Activity in HepG2-SR

Cell-based study · HepG2-SR [2]

In HepG2-SR, treatment with the compound for 48 h, using control vehicle as the control, yielded a half-maximal inhibitory concentration of 43.477 µM.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
half-maximal inhibitory concentration (IC50)IC50 43.477 µM[2]

Literature-Reported Treatment Conditions

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

Compound reported in the paper: TW-37

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

Materials and methods > Cell counting Kit-8 (CCK8) assay and combination index (CI) (S66, S70); Results > TW-37 suppresses MCM10 expression and enhances the efficacy of sorafenib in sorafenib-resistant HCC cells (S195)

half-maximal inhibitory concentration (IC50): half-maximal inhibitory concentration (IC50); comparator: control vehicle — Results > TW-37 suppresses MCM10 expression and enhances the efficacy of sorafenib in sorafenib-resistant HCC cells (S195)

Growth inhibition in WSU-pre-B-ALL

Cell-based study · WSU-pre-B-ALL [3]

WSU-pre-B-ALL samples received the study compound at concentrations up to 750 nM for 72 hr, with untreated samples as controls. The concentration producing 50% growth inhibition was 180 nM.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
50% growth inhibition (IC50)IC50 180 nM[3]

Literature-Reported Treatment Conditions

Treatment concentration
0.0–750 nM
Exposure duration
72 hr
Reported limits
Not stated in the sentences used: route, vehicle.
Methods and source locations

Compound reported in the paper: TW-37

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

Materials and methods > Effect of TW-37 on Growth of established cell lines and fresh lymphoma cells (S10, S12, S14); Results > Effect of TW-37 on growth of established malignant lymphoid cell lines and patient-derived lymphoma cells (S72); Figure 1 legend (S115)

50% growth inhibition (IC50): 50% growth inhibition (IC50); comparator: untreated samples — Results > Effect of TW-37 on growth of established malignant lymphoid cell lines and patient-derived lymphoma cells (S72)

In Vivo Studies

TW-37 was administered at 40 mg/kg via tail vein to female ICR-SCID mice bearing WSU-DLCL2 xenografts. Compared with diluent control, treatment produced a significant tumor growth delay of 10 days (p ≤ 0.01). [3]

Tumor growth delay in WSU-DLCL2 xenografts

Animal study · Four-week-old female ICR-SCID mice; WSU-DLCL2-bearing SCID mice; number of animals per group = 5 [3]

In female ICR-SCID mice bearing WSU-DLCL2 xenografts, TW-37 administered at 40 mg/kg via tail vein produced a significant tumor growth delay of 10 days compared with diluent control (p ≤ 0.01).

Measured endpoints — not treatment concentrations
EndpointReported resultReference
tumor growth delay (T-C)tumor growth delay (T-C) 10 days[3]

Conditions shared by the study groups

Route
via tail vein
Treatment course
three consecutive days
Vehicle
diluent
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
TW-37 40 mg/kgdiluent (as control)10 days; significant growth delay (p ≤ 0.01) compared with control[3]
TW-37 40 mg/kg
Model: Four-week-old female ICR-SCID mice; WSU-DLCL2-bearing SCID mice; number of animals per group = 5
Methods and source locations

Compound reported in the paper: TW-37

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

Materials and methods > SCID-mouse xenografts (S45); Materials and methods > Efficacy trial design for TW-37 (S53, S55); Results > In vivo efficacy of TW-37 in WSU-DLCL2-SCID mouse xenografts (S110, S112); Figure 7 legend (S150); Table 1 legend (S152); Table 1 (T1.h1, T1.r2)

tumor growth delay (T-C): tumor growth delay (T-C); comparator: diluent (as control) — Results > In vivo efficacy of TW-37 in WSU-DLCL2-SCID mouse xenografts (S110, S112); Table 1 (T1.h1, T1.r2)

TW-37 40 mg/kg · Results > In vivo efficacy of TW-37 in WSU-DLCL2-SCID mouse xenografts (S110, S112); Figure 7 legend (S150); Table 1 legend (S152)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 877877-35-5
Applications Bcl-2 inhibitor
Formula C33H35NO6S
Molecular Weight 573.7
SMILES
CC(C)C1=CC=CC=C1CC2=C(C(=C(C(=C2)C(=O)NC3=CC=C(C=C3)S(=O)(=O)C4=CC=CC=C4C(C)(C)C)O)O)O

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 110 mg/mL (191.73 mM)
Water Insoluble
Ethanol 4 mg/mL (6.97 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
28 mg/mL
Vehicle
30% propylene glycol, 5% Tween 80, 65% D5W

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] Wang H, Liu J, Yang X, et al. Optimal Hypoxia Mimetic Small Molecules for Enhancing Angiogenic Properties of Stem Cells From Human Exfoliated Deciduous Teeth. Int Endod J (2026). PMID: 42227314 DOI: 10.1111/iej.70191 Source material
  2. [2] Zhang Z, Liang L, Li Y, et al. Targeting MCM10 disrupts cancer stemness and counteracts sorafenib resistance in hepatocellular carcinoma. Cancer Gene Ther (2025). PMID: 40750706 DOI: 10.1038/s41417-025-00946-0 Source material
  3. [3] Al-Katib AM, Sun Y, Goustin AS, et al. SMI of Bcl-2 TW-37 is active across a spectrum of B-cell tumors irrespective of their proliferative and differentiation status. J Hematol Oncol (2009). PMID: 19220884 DOI: 10.1186/1756-8722-2-8 Source material

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