Cat. No.: HY-15322

PRT062607

Name: PRT062607
Brand: MedChemExpress
SKU: HY-15322
Price: 198.00 USD
Availability: InStock
Rating: 5 (5 reviews)

(Synonyms: P505-15; PRT-2607; BIIB-057)

5 Cited Publications

Customer Review

Based on 5 publication(s) in Google Scholar

PRT062607 (P505-15; PRT-2607) is an orally active ATP-competitive Syk inhibitor with an IC₅₀ value of 1 nM, and exhibits at least 80-fold selectivity over other kinases. PRT062607 blocks B cell antigen receptor-mediated activation, Fcε receptor 1-mediated basophil degranulation and microglial phagocytosis, and induces caspase-dependent apoptosis and microglial death. PRT062607 inhibits tumor growth and peripheral nerve injury-induced mechanical allodynia, and prevents neuronal loss. PRT062607 can be used in research related to rheumatoid arthritis, chronic lymphocytic leukemia, non-Hodgkin's lymphoma, neurodegenerative diseases and neuropathic pain.

For research use only. We do not sell to patients.

Purity : 99.38%
CAS No.: 1370261-96-3
Formula: C₁₉H₂₃N₉O
Molecular Weight:393.45

Storage:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month

PRT062607 Chemical Structure

CAS No.: 1370261-96-3

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Top Publications Citing

Use of MCE Products

Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- Cellular Effect
- In Vitro
- Parmacokinetics
- In Vivo
- Clinical Trial
Chemical Information
Publications (5)
Solvent & Solubility
- In Vitro
- In Vivo
Protocols (11)
Purity & Documentation
References
Help & FAQs
Classifications
Bioz

Biological Activity

Description

All Caspase Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
Bone marrow cell	IC₅₀	5853 nM Compound: 1, BIB-057	Cytotoxicity against C57BL/6 mouse bone marrow cells assessed as growth inhibition preincubated for 4 days followed by [3H]-thymidine addition measured after 5 hrs by betaplate counting analysis Cytotoxicity against C57BL/6 mouse bone marrow cells assessed as growth inhibition preincubated for 4 days followed by [3H]-thymidine addition measured after 5 hrs by betaplate counting analysis	[PMID: 25633741]
Bone marrow cell	IC₅₀	5853 nM Compound: 1, BIIB-057	Inhibition of IL3 dependent proliferation in C57/B16 mouse bone marrow cells using [3H]thymidine by liquid scintillation counting Inhibition of IL3 dependent proliferation in C57/B16 mouse bone marrow cells using [3H]thymidine by liquid scintillation counting	[PMID: 24726806]
CHO	IC₅₀	8600 nM Compound: 1, BIB-057	Inhibition of human ERG expressed in CHO cells by automated Qpatch clamp assay Inhibition of human ERG expressed in CHO cells by automated Qpatch clamp assay	[PMID: 25633741]
Jurkat	IC₅₀	1805 nM Compound: 1, BIB-057	Inhibition of ZAP70 in anti-CD3 stimulated human Jurkat T cells assessed as SLP76 phosphorylation at Y128 preincubated for 30 mins followed by anti-CD3 stimulation measured after 2 mins by FACS analysis Inhibition of ZAP70 in anti-CD3 stimulated human Jurkat T cells assessed as SLP76 phosphorylation at Y128 preincubated for 30 mins followed by anti-CD3 stimulation measured after 2 mins by FACS analysis	[PMID: 25633741]
Ramos	IC₅₀	0.223 μM Compound: 2	Inhibition of SYK in human Ramos cells Inhibition of SYK in human Ramos cells	[PMID: 23350847]
Ramos	IC₅₀	0.223 μM Compound: PRT062607	Cytotoxicity against human Ramos cells Cytotoxicity against human Ramos cells	[PMID: 23151054]
Ramos	IC₅₀	178 nM Compound: 1, BIIB-057	Inhibition of Syk in anti IgM-stimulated human Ramos cells assessed as BLNK phosphorylation by cellular assay Inhibition of Syk in anti IgM-stimulated human Ramos cells assessed as BLNK phosphorylation by cellular assay	[PMID: 24726806]

In Vitro

PRT062607 potently inhibits purified Syk in FRET kinase assays containing 15 and 100 μM ATP, with IC₅₀ values of 2.1 and 6 nM^[1].
PRT062607 (0.01-2.5 μM; 1.5 h) specifically inhibits BCR-mediated Syk-dependent BLNK Tyr84 phosphorylation in SUDHL4 cells, with an IC₅₀ of 0.16-0.4 μM^[1].
PRT062607 potently inhibits BCR-mediated Syk-dependent ERK Tyr204 phosphorylation in Ramos cells with an IC₅₀ of 50 nM; at concentrations up to 2 μM, this compound does not affect non-Syk-dependent, PMA-mediated ERK phosphorylation^[1].
PRT062607 (P505-15) (0-6 μM; 3 days) selectively inhibits the proliferation of Syk-dependent TEL-Syk Ba/F3 cells, with an IC₅₀ of 120 nM^[1].
PRT062607 (0-4 μM; 40 min) potently inhibits Syk-dependent BCR-mediated ERK Tyr204 phosphorylation in human whole blood B cells, with a mean IC₅₀ of 0.27 μM^[1].
PRT062607 (0-4 μM; 16.5 h) potently inhibits Syk-dependent BCR-mediated B cell activation (CD69 upregulation) in human whole blood, with a mean IC₅₀ of 0.28 μM^[1].
PRT062607 (0-4 μM; 1.25 h) potently inhibits Syk-dependent FcεR1-mediated basophil degranulation in human whole blood, with a mean IC₅₀ of 0.15 μM^[1].
PRT062607 (2 μM; 30 min) inhibits anti-IgM-induced autophosphorylation of SYK in Ramos human non-Hodgkin's lymphoma B cells^[2].
PRT062607 (0.02-2 μM; 30 min) inhibits anti-IgM-induced phosphorylation of ERK and AKT in the human non-Hodgkin's lymphoma B cell line Ramos in a concentration-dependent manner, with an IC₅₀ of approximately 50 nM, and achieves complete inhibition at 250 nM^[2].
PRT062607 (1-3 μM; 72 hours) induces apoptosis in human non-Hodgkin's lymphoma B cell lines SU-DHL4, SU-DHL6 and Ramos with functional BCR signaling, but exerts no such effect in BCR/BLNK-deficient Toledo/Karpas-422 cell lines or primary human B cells; PRT062607 (1 μM; 24 hours) induces apoptosis in SU-DHL6 cells mixed with whole blood, while primary B cells remain unaffected^[2].
PRT062607 (0.01-1 μM; 30 min) concentration-dependently inhibits BCR-induced AKT phosphorylation in primary human chronic lymphocytic leukemia (CLL) cells, with complete inhibition achieved at concentrations ranging from 0.3 to 1 μM^[2].
PRT062607 (10 nM-10 μM; 72 h) reduces cell viability by 36% in primary human chronic lymphocytic leukemia (CLL) samples, including high-risk samples with 17p deletion, 11q deletion or unmutated IgVh, with an IC₅₀ < 3 μM in responsive samples^[2].
PRT062607 (10 nM-10 μM; 72 h) acts synergistically with fludarabine to reduce the viability of primary human chronic lymphocytic leukemia (CLL) cells, and a fludarabine hyporeactive effect is observed at lower fludarabine concentrations^[2].
PRT062607 (10 μM; 3 d) completely blocks LPS (HY-D1056)-induced neuronal loss as well as spontaneous age-related neuronal loss in primary rat cerebellar neuron-glia cultures^[3].
PRT062607 (10 μM; 3 d) significantly depletes microglia and induces microglial death in primary rat cerebellar neuron-glia cultures without LPS treatment, but does not deplete microglia in LPS-treated cultures^[3].
PRT062607 (10 μM; 24 h) induces significant microglial necrosis and apoptotic cell death, and reduces total cell density in primary rat cortical microglia^[3].
PRT062607 (10 μM; overnight) reduces the phagocytosis of 5 μm microspheres by primary rat cortical microglia under both resting and LPS-activated conditions^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.

Western Blot Analysis^[1]

View Protocol

Cell Line:

SUDHL4 human non-Hodgkin's lymphoma B cell line
Concentration:

0.01, 0.025, 0.064, 0.16, 0.4, 1 and 2.5 μM
Incubation Time:

1 h (pretreatment); 30 min (stimulation)
Result:

Inhibited BCR-mediated BLNK Tyr84 phosphorylation in a concentration-dependent manner, with an IC₅₀ range of 0.16-0.4 μM.
Did not inhibit BCR-mediated Syk Tyr352 phosphorylation at concentrations up to 2.5 μM.

Cell Viability Assay^[1]

View Protocol

Cell Line:

Ba/F3 mouse pro-B cell line stably expressing TEL-Syk
Concentration:

0.074, 0.22, 0.66, 2 and 6 μM
Incubation Time:

3 days
Result:

Selectively inhibited proliferation of the TEL-Syk-expressing Ba/F3 cell line with an IC₅₀ of 120 ± 5 nM.
Did not inhibit proliferation of Ba/F3 cell lines expressing TEL-JAK1, TEL-JAK2, TEL-JAK3, TEL-Tyk2, or TEL-Zap70 at 2 μM.

Western Blot Analysis^[2]

View Protocol

Cell Line:

Ramos human non-Hodgkin lymphoma B-cell line
Concentration:

2 μM
Incubation Time:

30 minutes (preincubation)
Result:

Significantly reduced SYK autophosphorylation at the Y525/526 sites compared to stimulated, untreated cells.

Apoptosis Analysis^[2]

View Protocol

Cell Line:

SU-DHL4, SU-DHL6, Ramos, Toledo, and Karpas-422 human non-Hodgkin lymphoma B-cell lines; primary human B-cells
Concentration:

1 μM (24 h whole blood experiment); 1 μM, 3 μM (72 h apoptosis assay)
Incubation Time:

24 h (whole blood experiment); 72 h (apoptosis assay)
Result:

Induced apoptosis (measured by active caspase-3 cleavage) in BCR-signaling competent cell lines SU-DHL4, SU-DHL6, and Ramos, but not in BCR-deficient Toledo or BLNK-deficient Karpas-422 lines.
Induced apoptosis in SU-DHL6 cells mixed with heparinized human whole blood, while primary B-cells did not undergo apoptosis.

Parmacokinetics

Species	Dose	Route	T_1/2	T_max	C_min	AUC	C_max
Mice^[2]	10 mg/kg	p.o.	/	1.5 h	45 nM	738 ng·h/mL	/
Mice^[2]	15 mg/kg	p.o.	/	1.5 h	69 nM	1671 ng·h/mL	893 nM
Mice^[2]	20 mg/kg	p.o.	/	4.0 h	102 nM	3191 ng·h/mL	1484 nM
Mice^[2]	1 mg/kg	i.v.	3.9 h	/	/	/	/

In Vivo

PRT062607 (5-30 mg/kg; p.o.; twice daily; for 10-15 days) dose-dependently inhibits joint inflammation in collagen antibody-induced arthritis models of mice and rats^[1].
PRT062607 (15 mg/kg; p.o.; twice daily; 5 days) significantly inhibits B cell receptor (BCR)-induced splenomegaly and marginal B cell zone expansion in mice^[2].
PRT062607 (10-20 mg/kg; p.o.; twice daily; 5 weeks) significantly inhibits the growth of Ramos NHL tumors in NOD/SCID mice^[2].
PRT062607 (4.5 mg per rat; intrathecal injection; single administration) significantly reverses mechanical allodynia induced by spared nerve injury in rats^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

BALB/c (female)^[1]
Dosage:

5 mg/kg; 15 mg/kg; 30 mg/kg
Administration:

p.o.; b.i.d.; 10 days
Result:

Produced average paw inflammation score inhibitions of 12%, 44%, and 87% respectively, with corresponding average plasma concentrations of 0.38, 0.95, and 1.47 μM.
Significantly reduced blinded histopathology scores and hind paw ankle thickness in the 15 and 30 mg/kg dose groups compared with vehicle controls.
Rendered joint structure indistinguishable from normal naive mice at 30 mg/kg, with no intra-articular neutrophils, fibrin, or synovial tissue damage.

Animal Model:

Lewis (female, 7-week-old)^[1]
Dosage:

5 mg/kg; 10 mg/kg; 15 mg/kg
Administration:

p.o.; b.i.d.; 15 days
Result:

Completely suppressed inflammation in 7 of 8 rats at 15 mg/kg, resulting in a mean inflammation score of 0.63 with an average plasma concentration of 1.34 μM.
Produced a significantly efficacious reduction in inflammation at 10 mg/kg with an average plasma concentration of 0.72 μM.
Significantly reduced blinded histopathology scores and hind paw ankle thickness in the 15 mg/kg dose group compared with vehicle controls.
Rendered joint morphology indistinguishable from normal naive rats at 15 mg/kg, with no inflammatory infiltrate, synovial hyperplasia, or cartilage erosion.

Animal Model:

Balb/c (5 per group)^[2]
Dosage:

15 mg/kg
Administration:

p.o.; twice daily; 5 days
Result:

Reduced average spleen weight from ~0.17 g to ~0.12 g.
Corrected the expansion of the marginal B-cell zone observed in vehicle-treated anti-IgD mice.

Animal Model:

NOD/SCID (15 per group)^[2]
Dosage:

10 mg/kg; 15 mg/kg; 20 mg/kg
Administration:

p.o.; twice daily; until study termination
Result:

Reduced average tumor weight.
Sustained steady-state tumor concentrations above 63 nM (10 mg/kg), 176 nM (15 mg/kg), and 325 nM (20 mg/kg) over the entire dosing interval.
Increased lymphocyte counts in 15 mg/kg group; no reductions in any leukocyte subsets across all dose groups.

Animal Model:

Sprague Dawley (male and female, 7-8 weeks old, n=6 per sex per treatment group)^[4]
Dosage:

4.5 mg
Administration:

intrathecal injection; single injection
Result:

Significantly reversed SNI-induced mechanical pain hypersensitivity in both male and female rats.

Clinical Trial

NCT Number	Sponsor	Condition	Start Date	Phase A549
NCT01329991	Plexxikon\|		2011-05	PHASE1

Chemical Information

CAS No. 1370261-96-3
Appearance Solid
Molecular Weight 393.45
Formula C₁₉H₂₃N₉O
Color White to off-white
SMILES

NC(C1=CN=C(N[C@H]2[C@@H](N)CCCC2)N=C1NC3=CC=CC(N4N=CC=N4)=C3)=O
Synonyms

P505-15; PRT-2607; BIIB-057
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

Publications (5)

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Journal Impact Factor

Nat Commun

Human iPSC-based Modeling of Pulmonary Fibrosis Reveals p300/CBP Inhibition Suppresses Alveolar Transitional Cell State. [Abstract]

2026 Feb 12;17(1):1214. PMID: 41680175
Cell Death Dis

Activation of AKT via a dual mechanism enhances the susceptibility of melanoma cells to glucose deprivation. [Abstract]

2025 Aug 7;16(1):595. PMID: 40774947
Proc Natl Acad Sci U S A

Endocytosis triggers V-ATPase-SYK-mediated priming of cGAS activation and innate immune response. [Abstract]

2022 Oct 25;119(43):e2207280119. PMID: 36252040
Cell Rep

STUB1-VCP/p97 complex regulates mitophagy via fine-tuning of PINK1 levels. [Abstract]

2026 Mar 27;45(4):117183. PMID: 41903135
Int J Ophthalmol

NADPH oxidase 2 plays a protective role in experimental Aspergillus fumigatus keratitis in mice through killing fungi and limiting the degree of inflammation. [Abstract]

2022 Jul 18;15(7):1044-1052. PMID: 35919314

Solvent & Solubility

In Vitro:

DMSO : 100 mg/mL (254.16 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

2.5416 mL

12.7081 mL

25.4162 mL

5 mM

0.5083 mL

2.5416 mL

5.0832 mL

10 mM

0.2542 mL

1.2708 mL

2.5416 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Molarity Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

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Dilution Calculator

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In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline

Solubility: ≥ 5 mg/mL (12.71 mM); Clear solution

This protocol yields a clear solution of ≥ 5 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (50.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

Protocol 2

Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)

Solubility: ≥ 2.5 mg/mL (6.35 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

Protocol 3

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 2.5 mg/mL (6.35 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

Dosage Dosage
mg/kg
Animal Weight (Per Animal) Animal Weight (Per Animal)
g
Dosing Volume (Per Animal) Dosing Volume (Per Animal)
μL
Number of Animals Number of Animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

%
DMSO +

Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
%
+
+
%
Tween-80 + +
%
Saline +

The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).

Working solution concentration: 0.22 mg/mL

Protocols

All Cell Biology Animals and Diseases Signal Pathway Related

Phagocytosis Functional Assay
A phagocytosis functional assay measures the ability of phagocytic cells, such as neutrophils, macrophages, monocytes, or microglia/macrophages, to bind and internalize particulate targets including bacteria, yeast particles, beads, or myelin particles. Fluorescent flow-cytometry assays detect target uptake as fluorescence associated with gated phagocytes, while pH-sensitive dyes such as pHrodo increase signal in acidic phagosomal compartments and therefore preferentially report internalized particles rather than particles remaining outside the cell. Microscopy or high-content imaging can be used to confirm intracellular localization and, in some protocols, to follow uptake kinetics.
Collagen-Induced Arthritis
Collagen-induced arthritis (CIA) is an autoimmune murine model of rheumatoid arthritis in which immunization with type II collagen (CII) emulsified in an adjuvant induces a T cell- and autoantibody-driven inflammatory arthritis characterized by synovial hyperplasia, immune cell infiltration, and joint destruction. The model typically relies on genetically susceptible mouse strains (e. g. , DBA/1) and reproduces key features of human rheumatoid arthritis, including anti-collagen immune responses and progressive joint inflammation. Disease onset generally occurs within ~3-4 weeks after immunization, depending on antigen/adjuvant combinations and protocol variation. The immunopathology is driven by adaptive immune activation against CII, leading to systemic and local joint inflammation mediated by pro-inflammatory cytokines and effector immune cells, making CIA a standard preclinical platform for evaluating immunomodulatory and anti-arthritic interventions.
Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
Patient-Derived Xenograft (PDX)
Patient-derived xenograft (PDX) models are generated by engrafting primary human tumor tissue directly into immunodeficient mice, allowing in vivo propagation of patient tumor biology without initial in vitro adaptation. These models are used to preserve key histopathological and molecular characteristics of the original tumor and enable assessment of tumor growth dynamics and therapeutic response in a living organism. The biological readout is tumor engraftment and subsequent growth in the murine host, which reflects the ability of human tumor cells to survive, vascularize, and expand in an immunocompromised microenvironment.
Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
Patient-Derived Orthotopic Xenograft (PDOX)
Patient-derived orthotopic xenograft (PDOX) modeling implants fresh patient tumor tissue or patient-derived tumor cells into the anatomically corresponding organ or tissue site of immunodeficient mice, usually by surgical orthotopic implantation, to preserve patient tumor histology, local microenvironmental context, invasion, metastatic behavior, and treatment-response features better than subcutaneous implantation. PDOX readouts include tumor engraftment, orthotopic tumor growth, local invasion, metastasis, recurrence after resection, histologic similarity to the donor tumor, biomarker retention, molecular concordance, survival, and response or resistance to therapy. PDOX models are used for preclinical drug testing and individualized therapy evaluation, but engraftment success varies by tumor type and specimen quality.
Subcutaneous Cell-Line-Derived Xenograft
Subcutaneous cell-line-derived xenograft (CDX) models are established by implanting cultured human cancer cell lines into immunodeficient mice, where the injected cells form localized tumors that can be monitored in vivo as a measure of tumorigenic potential, growth kinetics, and treatment response. These models are widely used in oncology research because they allow reproducible tumor formation and enable comparative assessment of tumor growth between different cell lines or genetic manipulations in a controlled in vivo microenvironment. Subcutaneous implantation of cancer cells in immunodeficient mice is a standard approach for evaluating tumor growth behavior and therapeutic response across multiple cancer types, including prostate, esophageal, pancreatic, and colon cancer models.
Orthotopic Cell-Line Xenograft
Orthotopic cell-line xenograft models involve implantation of human cancer cell lines into the anatomically corresponding organ of immunodeficient mice to reproduce tumor growth within a native microenvironment, enabling more clinically relevant tumor behavior compared with subcutaneous models. These models are widely used because orthotopic placement better recapitulates tumor progression, including invasion and metastatic spread, which are often underrepresented in heterotopic implantation systems. Compared with conventional xenografts, orthotopic implantation is described as more technically complex but provides improved simulation of tumor-microenvironment interactions and metastatic behavior, making it particularly valuable for translational oncology research. Surgical orthotopic implantation approaches have been emphasized as enabling faithful reproduction of clinical cancer features, including metastasis and disease progression patterns that align with the tumor’s organ of origi

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (295 KB)
SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Coffey G, et al. Specific inhibition of spleen tyrosine kinase suppresses leukocyte immune function and inflammation in animal models of rheumatoid arthritis. J Pharmacol Exp Ther. 2012;340(2):350-359. [Content Brief]

[2]. Spurgeon SE, et al. The selective SYK inhibitor P505-15 (PRT062607) inhibits B cell signaling and function in vitro and in vivo and augments the activity of fludarabine in chronic lymphocytic leukemia. J Pharmacol Exp Ther. 2013;344(2):378-387. [Content Brief]

[3]. Birkle TJY, et al. Syk inhibitors protect against microglia-mediated neuronal loss in culture. Front Aging Neurosci. 2023;15:1120952. Published 2023 Mar 15. [Content Brief]

[4]. Ghazisaeidi S, et al. Conserved transcriptional programming across sex and species after peripheral nerve injury predicts treatments for neuropathic pain. Br J Pharmacol. 2023;180(21):2822-2836. [Content Brief]

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	2.5416 mL	12.7081 mL	25.4162 mL	63.5405 mL
	5 mM	0.5083 mL	2.5416 mL	5.0832 mL	12.7081 mL
	10 mM	0.2542 mL	1.2708 mL	2.5416 mL	6.3540 mL
	15 mM	0.1694 mL	0.8472 mL	1.6944 mL	4.2360 mL
	20 mM	0.1271 mL	0.6354 mL	1.2708 mL	3.1770 mL
	25 mM	0.1017 mL	0.5083 mL	1.0166 mL	2.5416 mL
	30 mM	0.0847 mL	0.4236 mL	0.8472 mL	2.1180 mL
	40 mM	0.0635 mL	0.3177 mL	0.6354 mL	1.5885 mL
	50 mM	0.0508 mL	0.2542 mL	0.5083 mL	1.2708 mL
	60 mM	0.0424 mL	0.2118 mL	0.4236 mL	1.0590 mL
	80 mM	0.0318 mL	0.1589 mL	0.3177 mL	0.7943 mL
	100 mM	0.0254 mL	0.1271 mL	0.2542 mL	0.6354 mL

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PRT062607

Publications Citing Use of MedChemExpress (MCE) PRT062607

All Caspase Isoforms