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Quality Control of [ 53123-88-9 ]

COA NMR CNMR HPLC LC-MS

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Product Citations Expand+

JAK and mTOR inhibitors prevent cytokine release while retaining T cell bispecific antibody in vivo efficacy

Leclercq, Gabrielle ; Haegel, Hélène ; Toso, Alberto , et al. J. ImmunoTher. Cancer,2022,10,e003766. DOI: 10.1136/jitc-2021-003766 PubMed ID: 35064010

Abstract: Background: T cell engaging therapies, like chimeric antigen receptor T cells and T cell bispecific antibodies (TCBs), efficiently redirect T cells towards tumor cells, facilitating the formation of a cytotoxic synapse and resulting in subsequent tumor cell killing, a process that is accompanied by the release of cytokines. Despite their promising efficacy in the clinic, treatment with TCBs is associated with a risk of cytokine release syndrome (CRS). The aim of this study was to identify small molecules able to mitigate cytokine release while retaining T cell-mediated tumor killing. Methods: By screening a library of 52 Food and Drug Administration approved kinase inhibitors for their impact on T cell proliferation and cytokine release after CD3 stimulation, we identified mTOR, JAK and Src kinases inhibitors as potential candidates to modulate TCB-mediated cytokine release at pharmacologically active doses. Using an in vitro model of target cell killing by human peripheral blood mononuclear cells, we assessed the effects of mTOR, JAK and Src kinase inhibitors combined with 2+1 T cell bispecific antibodies (TCBs) including CEA-TCB and CD19-TCB on T cell activation, proliferation and target cell killing measured by flow cytometry and cytokine release measured by Luminex. The combination of mTOR, JAK and Src kinase inhibitors together with CD19-TCB was evaluated in vivo in non-tumor bearing stem cell humanized NSG mice in terms of B cell depletion and in a lymphoma patient-derived xenograft (PDX) model in humanized NSG mice in terms of antitumor efficacy. Results: The effect of Src inhibitors differed from those of mTOR and JAK inhibitors with the suppression of CD19-TCB-induced tumor cell lysis in vitro, whereas mTOR and JAK inhibitors primarily affected TCB-mediated cytokine release. Importantly, we confirmed in vivo that Src, JAK and mTOR inhibitors strongly reduced CD19-TCB-induced cytokine release. In humanized NSG mice, continuous treatment with a Src inhibitor prevented CD19-TCB-mediated B cell depletion in contrast to mTOR and JAK inhibitors, which retained CD19-TCB efficacy. Ultimately, transient treatment with Src, mTOR and JAK inhibitors minimally interfered with antitumor efficacy in a lymphoma PDX model. Conclusions: Taken together, these data support further evaluation of the use of Src, JAK and mTOR inhibitors as prophylactic treatment to prevent occurrence of CRS.

Purchased from AmBeed: 159351-69-6 ; 941678-49-5 ; 302962-49-8 ; 162635-04-3 ; 53123-88-9

Cytokine release in the context of T cell bispecific antibody therapies: biological mechanisms and mitigation strategies

Leclercq, Gabrielle ; University of Basel,2021.

Abstract: T cell bispecific antibodies (TCBs) are a novel class of T cell engagers redirecting T cells towards tumor cells, facilitating the formation of a cytotoxic synapse and resulting in tumor celllysis. On-target activity of TCBs may come with a risk of Cytokine Release Syndrome (CRS), characterized by elevated levels of pro-inflammatory cytokines in the serum, such as IL-6, IL-1β, TNF-α or IFN-γ and over activation of immune cells. Besides, the expression of the tumorassociated antigen on healthy cells may induce off-tumor activity of the TCB and contribute to inflammation. Despite the use of step-up dosing, glucocorticoids, or tocilizumab to manage or prevent these safety liabilities, they remain the major dose-limiting toxicities associated with the treatment of T cell engagers, highlighting the need to develop preventive mitigation treatments. To this aim, we investigated the biological mechanisms and the chronology of events involved in TCB-mediated cytokine release and explored mitigation strategies that might retain profound treatment efficacy while reducing cytokine release. Using an in vitro co-culture of peripheral blood mononuclear cells (PBMCs) or total leukocytes(PBMCs + neutrophils) and target cells with the respective TCBs, or whole blood treated with a B cell depleting TCB, we confirmed the contribution of T cell and myeloid cells and revealed the role of neutrophils in the TCB-mediated cytokine release. In the same model, the use of anticytokine neutralizing antibodies provided insights into the chronology of events triggering the cascade of cytokines after TCB stimulation. Ultimately this work guided the evaluation of mitigation strategies directed against T-cell derived cytokine release by targeting kinases involved in signaling pathways downstream of the T cell receptor (TCR) after stimulation with TCBs. A novel small molecule-kinase inhibitors screen identified mTOR, JAK and Src inhibitors as candidates to switch-off T-cell derived cytokine release. We validated the effects of these kinase inhibitors and fine-tuned their effective doses in in vitro co-cultures of peripheral blood mononuclear cells (PBMCs) and tumor cells with the respective TCBs. In vivo, we used nontumor or tumor-bearing-humanized NSG mice to assess the effect of mTOR, JAK and Srcinhibitors on CD19-TCB-mediated cytokine release and anti-tumor efficacy. Altogether, we confirmed the biological mechanisms of the TCB-mediated cytokine cascade and revealed the contribution of neutrophils. Our work on kinase inhibitors highlights their differential activities on the inhibition of cytokine release and/or T cell cytotoxicity and demonstrates the decoupling between both mechanisms. Our data open new horizons for the prophylactic mitigation of CRS with the use of FDA approved mTOR and JAK inhibitors or the transient use of the Src inhibitor dasatinib. Finally, our results also indicate that dasatinib may serve as an “antidote” against adverse events related to the treatment with TCBs such as high grade CRS or unpredictable off-tumor activity of TCBs, a strategy which is now implemented the clinic.

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Product Details of [ 53123-88-9 ]

CAS No. :	53123-88-9	MDL No. :	MFCD00867594
Formula :	C₅₁H₇₉NO₁₃	Boiling Point :	-
Linear Structure Formula :	-	InChI Key :	QFJCIRLUMZQUOT-HPLJOQBZSA-N
M.W :	914.17	Pubchem ID :	5284616
Synonyms :	Sirolimus;AY-22989;D00753;C07909;SILA 9268A;SLM;RPM;RAP;RAPA;Wy 090217;NSC 226080;NSC-2260804;Rapamune	Chemical Name :	(3S,6R,7E,9R,10R,12R,14S,15E,17E,19E,21S,23S,26R,27R,34aS)-9,10,12,13,14,21,22,23,24,25,26,27,32,33,34,34a-Hexadecahydro-9,27-dihydroxy-3-[(1R)-2-[(1S,3R,4R)-4-hydroxy-3-methoxycyclohexyl]-1-methylethyl]-10,21-dimethoxy-6,8,12,14,20,26-hexamethyl-23,27-epoxy-3H-pyrido[2,1-c][1,4]oxaazacyclohentriacontine-1,5,11,28,29(4H,6H,31H)-pentone

Safety of [ 53123-88-9 ]

Signal Word:	Warning	Class:	N/A
Precautionary Statements:	P261-P305+P351+P338	UN#:	N/A
Hazard Statements:	H302-H315-H319	Packing Group:	N/A
GHS Pictogram:

Application In Synthesis of [ 53123-88-9 ]

* All experimental methods are cited from the reference, please refer to the original source for details. We do not guarantee the accuracy of the content in the reference.

Upstream synthesis route of [ 53123-88-9 ]
Downstream synthetic route of [ 53123-88-9 ]

[ 53123-88-9 ] Synthesis Path-Upstream 1~3

1
[ 75-21-8 ]
[ 53123-88-9 ]
[ 159351-69-6 ]

Yield	Reaction Conditions	Operation in experiment
6.9 g	With trifluorormethanesulfonic acid In toluene at 70℃; for 8 h; Autoclave	9.14 g rapamycin (0.01mol), 11g ethylene oxide (0.25 mol), 0.1 g trifluoromethanesulfonic acid, 30mL toluene was added to the autoclave after mixing, Warmed to 70 ° C, Maintaining 1.0 MPa pressure, the reaction was stopped after 8 hours, cooled to room temperature,The solvent was recovered under reduced pressure and the residue was purified by silica gel column chromatography (200-300 mesh silica gel,Eluent: ethyl acetate: petroleum ether = 20: 1),7.7 g 97.95percent of everolimus was obtained, which was purified by HP-20 resin column chromatography (eluent: acetonitrile: water = 65:35) 6.9 g of everolimus was obtained as a white solid, HPLC purity:99.6percent, Isomer content:0.12percent. Molar yield:72.0percent

Reference： [1] Patent: CN104876944, 2017, B, . Location in patent: Paragraph 0035-0050

2
[ 107-21-1 ]
[ 53123-88-9 ]
[ 159351-69-6 ]

Yield	Reaction Conditions	Operation in experiment
5.7 kg	Stage #1: With trifluoroacetic anhydride In tetrahydrofuran at 10℃; for 1.5 h; Inert atmosphere; Large scale Stage #2: With boron trifluoride diethyl etherate In tetrahydrofuran at 10℃; for 2 h; Large scale	620g of ethylene glycol and 6L of tetrahydrofuran were added to the reaction flask,Mix well to mix.The reaction temperature was controlled at 10 .Under nitrogen protection,1.41L trifluoroacetic anhydride was slowly added dropwise,Dropping is completed,Reaction for 1.5 hours,The reaction solution.9.14 kg of rapamycin was dissolved in 54 L of tetrahydrofuran,Added to the reaction solution,The reaction temperature was controlled at 10 .Slowly add 13ml boron trifluoride diethyl ether solution. Bi completed,The reaction was stirred for 2 hours. After the reaction is completed,60L saturated aqueous sodium bicarbonate solution was added,Stir wellThen suction filtered,To the filtrate was added 30 L of ethyl acetate,Liquid separation,The organic phase is washed with pure water until nearly neutral.The organic phase was dried over 500 g of anhydrous sodium sulfate for 2 hours, filtered,Concentrated under reduced pressure to a solventless outflow,A thick liquid. Column chromatography,The eluent is petroleum ether:Ethyl acetate = 1: 6. The collected effluent was concentrated under reduced pressure to give 6.3 kg of yellow foamy solid,Yield 66percent.A mixture of 26.8 L of methanol and ethyl acetate (v / v = 1/3) was added to the above yellow foamy solid,Stirring to dissolve,The temperature was controlled at 25 for 30 minutes,13.4 L cyclohexane was added dropwise,Bi completed,The temperature was controlled at 12 for 2 hours,Cool the feed liquid to about 0 slowly stirring 3h,Suction filtration,Drying at room temperature under vacuum gave 5.7 kg of a white solid,HPLC and mass spectrometry determined that the white solid was everolimus,Purity 98.1percent.

Reference： [1] Patent: CN106146535, 2016, A, . Location in patent: Paragraph 0037; 0038; 0039; 0040; 0041; 0042; 0043-0056

3
[ 53123-88-9 ]
[ 159351-69-6 ]

Reference： [1] Patent: WO2014/203185, 2014, A1,
[2] Patent: WO2016/20664, 2016, A1,
[3] Patent: CN105254646, 2016, A,
[4] Patent: CN105254646, 2016, A,
[5] Patent: CN105254646, 2016, A,
[6] Patent: CN105254646, 2016, A,
[7] Patent: WO2016/207205, 2016, A1,
[8] Patent: CN106146536, 2016, A,

[ 53123-88-9 ] Synthesis Path-Downstream 1~5

1
[ 38222-83-2 ]
[ 53123-88-9 ]
[ 1111-92-8 ]
[ 3283-12-3 ]

Yield	Reaction Conditions	Operation in experiment
	With sodium hydrogencarbonate; In dichloromethane; ethyl acetate;	Dimethyl-phosphinic acid C-43 rapamycin ester To a cooled (0° C.) solution of rapamycin (0.1 g, 0.109 mmol) in 1.8 mL of dichloromethane was added 0.168 g (0.82 mmol) of 2,6-di-t-butyl-4-methyl pyridine, under a stream of N2, followed immediately by a solution of dimethylphosphinic chloride (0.062 g, 0.547 mmol) in 0.2 mL of dichloromethane. The slightly yellow reaction solution was stirred at 0° C., under an atmosphere of N2, for 3.5 h (reaction monitored by TLC). The cold (0° C.) reaction solution was diluted with ~20 mL EtOAc then transferred to a separatory funnel containing EtOAc (150 mL) and saturated NaHCO3 (100 mL). Upon removing the aqueous layer, the organic layer was washed successively with ice cold 1N HCl (1100 mL), saturated NaHCO3(1100 mL), and brine (1*100 mL), then dried over MgSO4 and concentrated. The crude product was purified by silica gel flash chromatography (eluted with 1:10:3:3 MeOH/DCM/EtOAc/hexane) to provide 0.092 g of a white solid: 1H NMR (300 MHz, CDCl3) d 4.18 (m, 1H), 4.10 (m, 1H), 3.05 (m, 1H), 1.5 (m, 6H); 31P NMR (121 MHz, CDCl3) d 53.6; 1013 m/z (M+Na).
	With sodium hydrogencarbonate; In dichloromethane; ethyl acetate;	Dimethyl-phosphinic acid C-43 rapamycin ester To a cooled (0° C.) solution of rapamycin (0.1 g, 0.109 mmol) in 1.8 mL of dichloromethane was added 0.168 g (0.82 mmol) of 2,6-di-t-butyl-4-methyl pyridine, under a stream of N2, followed immediately by a solution of dimethylphosphinic chloride (0.062 g, 0.547 mmol) in 0.2 mL of dichloromethane. The slightly yellow reaction solution was stirred at 0° C., under an atmosphere of N2, for 3.5 h (reaction monitored by TLC). The cold (0° C.) reaction solution was diluted with ~20 mL EtOAc then transferred to a separatory funnel containing EtOAc (150 mL) and saturated NaHCO3 (100 mL). Upon removing the aqueous layer, the organic layer was washed successively with ice cold 1N HCl (1100 mL), saturated NaHCO3(1100 mL), and brine (1*100 mL), then dried over MgSO4 and concentrated. The crude product was purified by silica gel flash chromatography (eluted with 1:10:3:3 MeOH/DCM/EtOAc/hexane) to provide 0.092 g of a white solid: 1H NMR (300 MHz, CDCl3) d 4.18 (m, 1H), 4.10 (m, 1H), 3.05 (m, 1H), 1.51 (m, 6H); 31P NMR (121 MHz, CDCl3) d 53.6; 1013 m/z (M+Na).
	With sodium hydrogencarbonate; In dichloromethane; ethyl acetate;	EXAMPLE 2Dimethyl-Phosphinic Acid C-43 Rapamycin EsterTo a cooled (0° C.) solution of rapamycin (0.1 g, 0.109 mmol) in 1.8 mL of dichloromethane was added 0.168 g (0.82 mmol) of 2,6-di-t-butyl-4-methyl pyridine, under a stream of N2, followed immediately by a solution of dimethylphosphinic chloride (0.062 g, 0.547 mmol) in 0.2 mL of dichloromethane.The slightly yellow reaction solution was stirred at 0° C., under an atmosphere of N2, for 3.5 h (reaction monitored by TLC).The cold (0° C.) reaction solution was diluted with ~20 mL EtOAc then transferred to a reparatory funnel containing EtOAc (150 mL) and saturated NaHCO3 (100 mL).Upon removing the aqueous layer, the organic layer was washed successively with ice cold 1N HCl (1100 mL), saturated NaHCO3(1100 mL), and brine (1*100 mL), then dried over MgSO4 and concentrated.The crude product was purified by silica gel flash chromatography (eluted with 1:10:3:3 MeOH/DCM/EtOAc/hexane) to provide 0.092 g of a white solid: 1H NMR (300 MHz, CDCl3) delta4.18 (m, 1H), 4.10 (m, 1H), 3.05 (m, 1H), 1.51 (m, 6H); 31P NMR (121 MHz, CDCl3) delta 53.6; 1013 m/z (M+Na).

Reference： [1]Patent: US2003/220297,2003,A1
[2]Patent: US2005/32825,2005,A1
[3]Patent: US2012/289481,2012,A1

2
[ 53123-88-9 ]
[ 5736-06-1 ]
rapamycin 42-ester with 2,2-dimethyl[1,3]dioxalane-4-carboxylic acid [ No CAS ]
rapamycin 31,42-dester with 2,2-dimethyl[1,3]dioxalane-4-carboxylic acid [ No CAS ]

Reference： [1]Patent: EP1266899,2002,A2 .Location in patent: Example 5,6

3
[ 391-12-8 ]
[ 22979-35-7 ]
[ 53123-88-9 ]
C₆₉H₉₁F₃N₂O₁₇ [ No CAS ]

Yield	Reaction Conditions	Operation in experiment
86%		Weigh rapamycin (0.05mmol), isatin 3m (0.10mmol) and rhodium octanoate dimer(0.0005mmo),They were placed in a reaction flask, 2.0 mL of dry dichloromethane was added, and after stirring at room temperature for 5 minutes,Phenyldiazo 2a (0.10 mmol) was weighed and dissolved in dry dichloromethane (1.0 mL), and slowly added dropwise to the reaction system (about 1 hour), and stirring was continued for half an hour.The solvent was removed by rotary distillation to give a crude product. The rapamycin analog I-m was obtained by column chromatography (eluent: petroleum ether: ethyl acetate = 1:10 to 1:4).The yield was 86percent.

Reference： [1]Patent: CN109776571,2019,A .Location in patent: Paragraph 0070-0073

4
[ 391-12-8 ]
[ 22979-35-7 ]
[ 53123-88-9 ]
40-O-(1-(3-hydroxy-2-oxo-7-(trifluoromethyl)indolin-3-yl)-2-methoxy-2-oxo-1-phenylethoxy)rapamycin [ No CAS ]
40-O-(1-(3-hydroxy-2-oxo-7-(trifluoromethyl)indolin-3-yl)-2-methoxy-2-oxo-1-phenylethoxy)rapamycin [ No CAS ]

Reference： [1]European Journal of Organic Chemistry,2019,vol. 2019,p. 2914 - 2918

5
[ 3386-18-3 ]
[ 53123-88-9 ]
(21E,23E,25E,26E,46R,47S,48R,49R,51S,53S,56S,57R,58R,67R)-57,67-dihydroxy-55-[2-[2-[2-[2-[2-[2-[2-[2-(2-hydroxyethoxy)ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]-56-[(1R)-2-[(1S,3R,4R)-4-hydroxy-3-methoxy-cyclohexyl]-1-methyl-ethyl]-58-methoxy-46,47,48,49,59,60-hexamethyl-78,79-dioxa-68-azatricyclohexatriaconta-21,23,25⁽⁵⁹⁾,26⁽⁶⁰⁾-tetraene-61,62,63,64,65-pentone [ No CAS ]

Yield	Reaction Conditions	Operation in experiment
16%	With toluene-4-sulfonic acid; In tetrahydrofuran; at 10 - 35℃; for 18h;Inert atmosphere;	To a solution of rapamycin (0.5 g, 0.547 mmol) in THF (15 mL) was added 4- methylbenzenesulfonic acid (0.47 g, 2.73 mmol) and <strong>[3386-18-3]nonaethylene glycol</strong> (2.27 g, 5.47 mmol) at 10 C. The reaction was stirred at 30C for 18 h under N2 then quenched with aq. NaHCO3 and extracted with EtOAc (60 mL× 3). The combined organic layers were washed with water (50 mL), brine (50 mL), dried over anhydrous Na2SO4, filtered and concentrated. The residue was purified by reverse phase chromatography (C18, CH3CN:H2O = 63:37) to provide (21E,23E,25E,26E,46R,47S,48R,49R,51S,53S,56S,57R,58R,67R)-57,67-dihydroxy-55-[2-[2- [2-[2-[2-[2-[2-[2-(2-hydroxyethoxy)ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy] ethoxy]-56-[(1R)-2-[(1S,3R,4R)-4-hydroxy-3-methoxy-cyclohexyl]-1-methyl-ethyl]-58- methoxy-46,47,48,49,59,60-hexamethyl-78,79-dioxa-68-azatricyclohexatriaconta- 21,23,25(59),26(60)-tetraene-61,62,63,64,65-pentone (I-97: 111 mg, 16% yield) as a white solid. ESI-MS (EI+, m/z): 1318.9 [M+Na]+. 1H NMR (500 MHz, CDCl3) d 6.50- 5.79 (m, 4H), 5.64- 5.06 (m, 4H), 4.89 (d, J = 53.5 Hz, 1H), 4.51- 3.94 (m, 2H), 3.75- 3.18 (m, 46H), 3.02- 2.86 (m, 2H), 2.82- 2.61 (m, 3H), 2.39- 2.18 (m, 2H), 2.20- 1.91 (m, 6H), 1.78- 1.54 (m, 16H), 1.51- 1.19 (m, 11H), 1.09- 0.82 (m, 17H), 0.74- 0.62 (m, 1H).

Reference： [1]Patent: WO2019/241789,2019,A1 .Location in patent: Paragraph 00532-00533

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P370 + P380	In case of fire: Evacuate area.
P370 + P380 + P375	In case of fire: Evacuate area. Fight fire remotely due to the risk of explosion.
P371 + P380 + P375	In case of major fire and large quantities: Evacuate area. Fight fire remotely due to the risk of explosion.
Storage
Code	Phrase
P401
P402	Store in a dry place.
P403	Store in a well-ventilated place.
P404	Store in a closed container.
P405	Store locked up.
P406	Store in corrosive resistant/ container with a resistant inner liner.
P407	Maintain air gap between stacks/pallets.
P410	Protect from sunlight.
P411
P412	Do not expose to temperatures exceeding 50 oC/ 122 oF.
P413
P420	Store away from other materials.
P422
P402 + P404	Store in a dry place. Store in a closed container.
P403 + P233	Store in a well-ventilated place. Keep container tightly closed.
P403 + P235	Store in a well-ventilated place. Keep cool.
P410 + P403	Protect from sunlight. Store in a well-ventilated place.
P410 + P412	Protect from sunlight. Do not expose to temperatures exceeding 50 oC/122oF.
P411 + P235	Keep cool.
Disposal
Code	Phrase
P501	Dispose of contents/container to ...
P502	Refer to manufacturer/supplier for information on recovery/recycling

Physical hazards
Code	Phrase
H200	Unstable explosive
H201	Explosive; mass explosion hazard
H202	Explosive; severe projection hazard
H203	Explosive; fire, blast or projection hazard
H204	Fire or projection hazard
H205	May mass explode in fire
H220	Extremely flammable gas
H221	Flammable gas
H222	Extremely flammable aerosol
H223	Flammable aerosol
H224	Extremely flammable liquid and vapour
H225	Highly flammable liquid and vapour
H226	Flammable liquid and vapour
H227	Combustible liquid
H228	Flammable solid
H229	Pressurized container: may burst if heated
H230	May react explosively even in the absence of air
H231	May react explosively even in the absence of air at elevated pressure and/or temperature
H240	Heating may cause an explosion
H241	Heating may cause a fire or explosion
H242	Heating may cause a fire
H250	Catches fire spontaneously if exposed to air
H251	Self-heating; may catch fire
H252	Self-heating in large quantities; may catch fire
H260	In contact with water releases flammable gases which may ignite spontaneously
H261	In contact with water releases flammable gas
H270	May cause or intensify fire; oxidizer
H271	May cause fire or explosion; strong oxidizer
H272	May intensify fire; oxidizer
H280	Contains gas under pressure; may explode if heated
H281	Contains refrigerated gas; may cause cryogenic burns or injury
H290	May be corrosive to metals
Health hazards
Code	Phrase
H300	Fatal if swallowed
H301	Toxic if swallowed
H302	Harmful if swallowed
H303	May be harmful if swallowed
H304	May be fatal if swallowed and enters airways
H305	May be harmful if swallowed and enters airways
H310	Fatal in contact with skin
H311	Toxic in contact with skin
H312	Harmful in contact with skin
H313	May be harmful in contact with skin
H314	Causes severe skin burns and eye damage
H315	Causes skin irritation
H316	Causes mild skin irritation
H317	May cause an allergic skin reaction
H318	Causes serious eye damage
H319	Causes serious eye irritation
H320	Causes eye irritation
H330	Fatal if inhaled
H331	Toxic if inhaled
H332	Harmful if inhaled
H333	May be harmful if inhaled
H334	May cause allergy or asthma symptoms or breathing difficulties if inhaled
H335	May cause respiratory irritation
H336	May cause drowsiness or dizziness
H340	May cause genetic defects
H341	Suspected of causing genetic defects
H350	May cause cancer
H351	Suspected of causing cancer
H360	May damage fertility or the unborn child
H361	Suspected of damaging fertility or the unborn child
H361d	Suspected of damaging the unborn child
H362	May cause harm to breast-fed children
H370	Causes damage to organs
H371	May cause damage to organs
H372	Causes damage to organs through prolonged or repeated exposure
H373	May cause damage to organs through prolonged or repeated exposure
Environmental hazards
Code	Phrase
H400	Very toxic to aquatic life
H401	Toxic to aquatic life
H402	Harmful to aquatic life
H410	Very toxic to aquatic life with long-lasting effects
H411	Toxic to aquatic life with long-lasting effects
H412	Harmful to aquatic life with long-lasting effects
H413	May cause long-lasting harmful effects to aquatic life
H420	Harms public health and the environment by destroying ozone in the upper atmosphere

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[ CAS No. 53123-88-9 ] {[proInfo.proName]}

Quality Control of [ 53123-88-9 ]

Related Doc. of [ 53123-88-9 ]

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Product Details of [ 53123-88-9 ]

Safety of [ 53123-88-9 ]

Application In Synthesis of [ 53123-88-9 ]

[ 53123-88-9 ] Synthesis Path-Upstream 1~3

[ 53123-88-9 ] Synthesis Path-Downstream 1~5

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