PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
15634899-5	2005	C3aR and C5a receptor (C5aR) signaling was blocked using the nonpeptidic C3aR antagonist SB290157 and the neutralizing C5aR mAb 20/70 in a murine model of Aspergillus fumigatus extract induced pulmonary allergy.	SB 290157	89-97	complement component 3a receptor 1	Mus musculus	0-4
19684087-11	2009	On the other hand, SB290157 suppressed the increased expression of IL-1beta in the lung in this model, and the intratracheal administration of IL-1beta induced airway obstruction, airway hyperresponsiveness, and neutrophil infiltration in normal mice.	SB 290157	19-27	interleukin 1 beta	Mus musculus	67-75
19357704-4	2009	In agreement with the murine data, blockage of C3aR on human umbilical cord blood CD34(+) cells by C3aR antagonist SB290157 impairs their engraftment in non-obese diabetic/severe combined immunodeficient mice.	SB 290157	115-123	complement component 3a receptor 1	Mus musculus	47-51
19357704-4	2009	In agreement with the murine data, blockage of C3aR on human umbilical cord blood CD34(+) cells by C3aR antagonist SB290157 impairs their engraftment in non-obese diabetic/severe combined immunodeficient mice.	SB 290157	115-123	CD34 molecule	Homo sapiens	82-86
19357704-4	2009	In agreement with the murine data, blockage of C3aR on human umbilical cord blood CD34(+) cells by C3aR antagonist SB290157 impairs their engraftment in non-obese diabetic/severe combined immunodeficient mice.	SB 290157	115-123	complement C3a receptor 1	Homo sapiens	99-103
15944244-0	2005	Agonist activity of the small molecule C3aR ligand SB 290157.	SB 290157	51-60	complement C3a receptor 1	Homo sapiens	39-43
16154494-0	2005	The C3a receptor antagonist SB 290157 has agonist activity.	SB 290157	28-37	complement C3	Homo sapiens	4-7
15634899-5	2005	C3aR and C5a receptor (C5aR) signaling was blocked using the nonpeptidic C3aR antagonist SB290157 and the neutralizing C5aR mAb 20/70 in a murine model of Aspergillus fumigatus extract induced pulmonary allergy.	SB 290157	89-97	complement component 5a receptor 1	Mus musculus	9-21
15634899-5	2005	C3aR and C5a receptor (C5aR) signaling was blocked using the nonpeptidic C3aR antagonist SB290157 and the neutralizing C5aR mAb 20/70 in a murine model of Aspergillus fumigatus extract induced pulmonary allergy.	SB 290157	89-97	complement component 5a receptor 1	Mus musculus	23-27
15634899-5	2005	C3aR and C5a receptor (C5aR) signaling was blocked using the nonpeptidic C3aR antagonist SB290157 and the neutralizing C5aR mAb 20/70 in a murine model of Aspergillus fumigatus extract induced pulmonary allergy.	SB 290157	89-97	complement component 3a receptor 1	Mus musculus	73-77
14604969-3	2004	In this study, mobilization was induced with granulocyte colony-stimulating factor (G-CSF) in both C3-deficient (C3-/-) and C3a receptor-deficient (C3aR-/-) mice as well as in wild-type (wt) mice in the presence or absence of a C3aR antagonist, SB 290157.	SB 290157	245-254	colony stimulating factor 3 (granulocyte)	Mus musculus	84-89
14604969-4	2004	The data indicated (1) significantly increased G-CSF-induced mobilization in C3-/- and C3aR-/- mice compared with wt mice, (2) significantly accelerated and enhanced G-CSF-induced mobilization in wt, but not in C3-/- or C3aR-/-, mice treated with SB 290157, and (3) deposition of C3b/iC3b fragments onto the viable bone marrow (BM) cells of G-CSF-treated animals.	SB 290157	247-256	colony stimulating factor 3 (granulocyte)	Mus musculus	166-171
14604969-4	2004	The data indicated (1) significantly increased G-CSF-induced mobilization in C3-/- and C3aR-/- mice compared with wt mice, (2) significantly accelerated and enhanced G-CSF-induced mobilization in wt, but not in C3-/- or C3aR-/-, mice treated with SB 290157, and (3) deposition of C3b/iC3b fragments onto the viable bone marrow (BM) cells of G-CSF-treated animals.	SB 290157	247-256	colony stimulating factor 3 (granulocyte)	Mus musculus	166-171
14604969-8	2004	These data further suggest that the C3aR antagonist SB 290157 could be developed as a drug to mobilize HSPCs for transplantation.	SB 290157	52-61	complement component 3a receptor 1	Mus musculus	36-40
34150781-4	2021	Pharmacological targeting of the complement C3a receptor using SB290157 alleviated PDGF-D-induced neuroinflammation by blocking macrophage polarization and inhibited pathological choroidal neovascularization.	SB 290157	63-71	platelet derived growth factor D	Homo sapiens	83-89
11342658-6	2001	SB 290157 was selective for the C3aR in that it did not antagonize the C5aR or six other chemotactic G protein-coupled receptors.	SB 290157	0-9	complement C3a receptor 1	Rattus norvegicus	32-36
11342658-7	2001	Functional antagonism was not solely limited to the human C3aR; SB 290157 also inhibited C3a-induced Ca(2+) mobilization of RBL-2H3 cells expressing the mouse and guinea pig C3aRS: It potently inhibited C3a-mediated ATP release from guinea pig platelets and inhibited C3a-induced potentiation of the contractile response to field stimulation of perfused rat caudal artery.	SB 290157	64-73	RB transcriptional corepressor like 2	Rattus norvegicus	124-129
34921829-6	2022	Complement C3a peptide and C3aR antagonist (SB 290157, 10 mg/kg) were used to regulate the C3/C3aR pathway.	SB 290157	44-53	complement C3a receptor 1	Rattus norvegicus	94-98
33551801-0	2020	The "C3aR Antagonist" SB290157 is a Partial C5aR2 Agonist.	SB 290157	22-30	complement C3a receptor 1	Homo sapiens	5-9
33746964-8	2021	In isolated mitochondria from H2O2-treated cells C3a increased mitochondrial Ca2+ uptake, that could be inhibited by C3aR antagonism (SB290157), mitochondrial Ca2+ uniporter blocker (Ru360), and Galphai-protein inhibition (pertussis toxin, PTX); and inhibited mitochondrial repiration in an SB290157- and PTX-dependent manner.	SB 290157	134-142	complement C3	Homo sapiens	49-52
33746964-8	2021	In isolated mitochondria from H2O2-treated cells C3a increased mitochondrial Ca2+ uptake, that could be inhibited by C3aR antagonism (SB290157), mitochondrial Ca2+ uniporter blocker (Ru360), and Galphai-protein inhibition (pertussis toxin, PTX); and inhibited mitochondrial repiration in an SB290157- and PTX-dependent manner.	SB 290157	291-299	complement C3	Homo sapiens	49-52
33551801-13	2020	Given the reported immunomodulatory and anti-inflammatory activities of C5aR2 agonism, any function observed with SB290157 could be due to these off-target activities.	SB 290157	114-122	complement C5a receptor 2	Homo sapiens	72-77
33551801-0	2020	The "C3aR Antagonist" SB290157 is a Partial C5aR2 Agonist.	SB 290157	22-30	complement C5a receptor 2	Homo sapiens	44-49
33551801-3	2020	The non-peptide compound, SB290157, was originally reported in 2001 as the first C3aR antagonist.	SB 290157	26-34	complement C3a receptor 1	Homo sapiens	81-85
33551801-7	2020	Unfortunately, given the dearth of C3aR inhibitors, SB290157 still remains widely used to explore C3aR biology (>70 publications to date).	SB 290157	52-60	complement C3a receptor 1	Homo sapiens	98-102
33551801-8	2020	Given these issues, in the present study we aimed to further explore SB290157"s pharmacological selectivity by screening the drug against three human anaphylatoxin receptors, C3aR, C5aR1 and C5aR2, using cell models.	SB 290157	69-77	complement C3a receptor 1	Homo sapiens	175-179
33551801-8	2020	Given these issues, in the present study we aimed to further explore SB290157"s pharmacological selectivity by screening the drug against three human anaphylatoxin receptors, C3aR, C5aR1 and C5aR2, using cell models.	SB 290157	69-77	complement C5a receptor 1	Homo sapiens	181-186
33551801-8	2020	Given these issues, in the present study we aimed to further explore SB290157"s pharmacological selectivity by screening the drug against three human anaphylatoxin receptors, C3aR, C5aR1 and C5aR2, using cell models.	SB 290157	69-77	complement C5a receptor 2	Homo sapiens	191-196
33551801-9	2020	We identified that SB290157 exerts partial agonist activity at C5aR2 by mediating beta-arrestin recruitment at higher compound doses.	SB 290157	19-27	complement C5a receptor 2	Homo sapiens	63-68
33551801-10	2020	This translated to a functional outcome in both human and mouse primary macrophages, where SB290157 significantly dampened C5a-induced ERK signaling.	SB 290157	91-99	hemolytic complement	Mus musculus	123-126
33551801-10	2020	This translated to a functional outcome in both human and mouse primary macrophages, where SB290157 significantly dampened C5a-induced ERK signaling.	SB 290157	91-99	mitogen-activated protein kinase 1	Mus musculus	135-138
33551801-11	2020	We also confirmed that SB290157 acts as a potent agonist at human C3aR in transfected cells, but as an antagonist in primary human macrophages.	SB 290157	23-31	complement C3a receptor 1	Homo sapiens	66-70
32208992-5	2020	C3a receptor antagonist SB290157 suppressed renin and LXRalpha expression, with inhibition of nuclear translocation of LXRalpha during the differentiation of mouse MSCs to SMCs.	SB 290157	24-32	renin	Rattus norvegicus	44-49
31975437-2	2020	We previously reported that the C3aR antagonist SB290157 (C3aRA) is neuroprotective following transient but not permanent middle cerebral artery occlusion (MCAo).	SB 290157	48-56	complement C3a receptor 1	Homo sapiens	32-36
33174024-5	2020	SB290157 was used to block the activation of C3aR.	SB 290157	0-8	complement C3a receptor 1	Homo sapiens	45-49
32208992-5	2020	C3a receptor antagonist SB290157 suppressed renin and LXRalpha expression, with inhibition of nuclear translocation of LXRalpha during the differentiation of mouse MSCs to SMCs.	SB 290157	24-32	nuclear receptor subfamily 1, group H, member 3	Mus musculus	54-62
32020055-8	2020	Perturbation of C3a/C3aR signaling axis with either a small molecule inhibitor, SB290157, or reducing the levels of secreted C3a from liver-metastatic breast cancer cells by short hairpin RNAs, can abrogate the chemotactic response of iLDNs both in vitro and in vivo, respectively.	SB 290157	80-88	complement component 3a receptor 1	Mus musculus	20-24
24470120-5	2014	The osteoblastogenesis-stimulating activity present in osteoclast CM was inhibited by a specific antagonist of the C3a receptor (C3aR), SB290157.	SB 290157	136-144	complement C3a receptor 1	Homo sapiens	115-127
31814819-5	2019	Using a mouse model of stroke and two-photon microscopy, we aimed to attenuate poststroke phagocytosis of the dying but still viable neurons by using SB 290157, an antagonist of C3aR.	SB 290157	150-159	complement component 3a receptor 1	Mus musculus	178-182
31814819-6	2019	We found that intracortical administration of SB 290157 reduced the number of inflammatory microglial cells expressing ED1 and Iba1 antigens at the lesion site.	SB 290157	46-55	ectodysplasin-A	Mus musculus	119-122
31814819-6	2019	We found that intracortical administration of SB 290157 reduced the number of inflammatory microglial cells expressing ED1 and Iba1 antigens at the lesion site.	SB 290157	46-55	induction of brown adipocytes 1	Mus musculus	127-131
31814819-8	2019	We conclude that the C3aR antagonist, SB 290157, may be used in the future to limit the neuronal death by limiting secondary phagocytosis after stroke.	SB 290157	38-47	complement component 3a receptor 1	Mus musculus	21-25
30763805-7	2019	Alternative pathway (AP) activation or C3a-receptor (C3aR) and C5a-receptor (C5aR) engagement was inhibited during the repair phase only of CNV with the AP-inhibitor CR2-fH, a C3aR antagonist (N2-[(2,2-diphenylethoxy)acetyl]-l-arginine, TFA), or a C5a blocking antibody (CLS026), respectively.	SB 290157	193-235	complement component 3a receptor 1	Mus musculus	53-57
30763805-7	2019	Alternative pathway (AP) activation or C3a-receptor (C3aR) and C5a-receptor (C5aR) engagement was inhibited during the repair phase only of CNV with the AP-inhibitor CR2-fH, a C3aR antagonist (N2-[(2,2-diphenylethoxy)acetyl]-l-arginine, TFA), or a C5a blocking antibody (CLS026), respectively.	SB 290157	193-235	hemolytic complement	Mus musculus	63-66
30763805-7	2019	Alternative pathway (AP) activation or C3a-receptor (C3aR) and C5a-receptor (C5aR) engagement was inhibited during the repair phase only of CNV with the AP-inhibitor CR2-fH, a C3aR antagonist (N2-[(2,2-diphenylethoxy)acetyl]-l-arginine, TFA), or a C5a blocking antibody (CLS026), respectively.	SB 290157	193-235	complement component 5a receptor 1	Mus musculus	77-81
30763805-7	2019	Alternative pathway (AP) activation or C3a-receptor (C3aR) and C5a-receptor (C5aR) engagement was inhibited during the repair phase only of CNV with the AP-inhibitor CR2-fH, a C3aR antagonist (N2-[(2,2-diphenylethoxy)acetyl]-l-arginine, TFA), or a C5a blocking antibody (CLS026), respectively.	SB 290157	193-235	complement component 3a receptor 1	Mus musculus	176-180
30763805-7	2019	Alternative pathway (AP) activation or C3a-receptor (C3aR) and C5a-receptor (C5aR) engagement was inhibited during the repair phase only of CNV with the AP-inhibitor CR2-fH, a C3aR antagonist (N2-[(2,2-diphenylethoxy)acetyl]-l-arginine, TFA), or a C5a blocking antibody (CLS026), respectively.	SB 290157	193-235	hemolytic complement	Mus musculus	77-80
24974766-4	2014	A mouse model of skin sensitization was induced by TCE in the presence and absence of the C3aR antagonist SB 290157.	SB 290157	106-115	complement component 3a receptor 1	Mus musculus	90-94
24974766-11	2014	Pretreatment with SB 290157 resulted in more inflammatory infiltration in the liver, higher levels of AST, reduced C3aR expression on Kupffer cells, and decreased IL-4 levels while IFN-gamma remained unchanged.	SB 290157	18-27	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	102-105
24974766-11	2014	Pretreatment with SB 290157 resulted in more inflammatory infiltration in the liver, higher levels of AST, reduced C3aR expression on Kupffer cells, and decreased IL-4 levels while IFN-gamma remained unchanged.	SB 290157	18-27	complement component 3a receptor 1	Mus musculus	115-119
24974766-11	2014	Pretreatment with SB 290157 resulted in more inflammatory infiltration in the liver, higher levels of AST, reduced C3aR expression on Kupffer cells, and decreased IL-4 levels while IFN-gamma remained unchanged.	SB 290157	18-27	interleukin 4	Mus musculus	163-167
24974766-11	2014	Pretreatment with SB 290157 resulted in more inflammatory infiltration in the liver, higher levels of AST, reduced C3aR expression on Kupffer cells, and decreased IL-4 levels while IFN-gamma remained unchanged.	SB 290157	18-27	interferon gamma	Mus musculus	181-190
31903107-12	2020	Furthermore, the C3aR antagonist SB290157 decreased the number of microglia adhering to myelin (p<0.05), attenuated white matter injury and cognitive deficits in chronic hypoperfusion rats (p<0.05).	SB 290157	33-41	complement C3a receptor 1	Rattus norvegicus	17-21
30771350-5	2019	These effects were alleviated by C3a receptor antagonist SB290157 and were further validated by C3a receptor siRNA in OA-treated SH-SY5Y cells.	SB 290157	57-65	complement C3	Homo sapiens	33-36
30771350-6	2019	In addition, our results demonstrated that SB290157 markedly inhibited the activities of glycogen synthase kinase 3beta (GSK3beta), but had no effect on protein phosphatase 2A C subunit (PP2Ac) and cyclin-dependent kinases 5 (CDK5).	SB 290157	43-51	glycogen synthase kinase 3 beta	Homo sapiens	89-119
30771350-6	2019	In addition, our results demonstrated that SB290157 markedly inhibited the activities of glycogen synthase kinase 3beta (GSK3beta), but had no effect on protein phosphatase 2A C subunit (PP2Ac) and cyclin-dependent kinases 5 (CDK5).	SB 290157	43-51	glycogen synthase kinase 3 beta	Homo sapiens	121-129
30771350-6	2019	In addition, our results demonstrated that SB290157 markedly inhibited the activities of glycogen synthase kinase 3beta (GSK3beta), but had no effect on protein phosphatase 2A C subunit (PP2Ac) and cyclin-dependent kinases 5 (CDK5).	SB 290157	43-51	cyclin dependent kinase 5	Homo sapiens	198-224
30771350-6	2019	In addition, our results demonstrated that SB290157 markedly inhibited the activities of glycogen synthase kinase 3beta (GSK3beta), but had no effect on protein phosphatase 2A C subunit (PP2Ac) and cyclin-dependent kinases 5 (CDK5).	SB 290157	43-51	cyclin dependent kinase 5	Homo sapiens	226-230
25259874-2	2014	A flexible compound (N2-[(2,2-diphenylethoxy)acetyl]-l-arginine, 4), known as a weak C3aR antagonist (IC50 muM), was transformed here into potent agonists (EC50 nM) of human macrophages (Ca(2+) release in HMDM) by incorporating aromatic heterocycles.	SB 290157	21-63	complement C3a receptor 1	Homo sapiens	85-89
25259874-2	2014	A flexible compound (N2-[(2,2-diphenylethoxy)acetyl]-l-arginine, 4), known as a weak C3aR antagonist (IC50 muM), was transformed here into potent agonists (EC50 nM) of human macrophages (Ca(2+) release in HMDM) by incorporating aromatic heterocycles.	SB 290157	21-63	latexin	Homo sapiens	107-110
24470120-5	2014	The osteoblastogenesis-stimulating activity present in osteoclast CM was inhibited by a specific antagonist of the C3a receptor (C3aR), SB290157.	SB 290157	136-144	complement C3a receptor 1	Homo sapiens	129-133
24470120-7	2014	C3 gene expression in bone was increased in the high bone turnover states of ovariectomy (OVX) or a receptor activator of NF-kappaB ligand (RANKL) injection, and blocking the action of C3a with the daily administration of SB290157 resulted in the attenuation of bone formation elevated by OVX and the exacerbation of bone loss.	SB 290157	222-230	complement C3	Homo sapiens	0-2
24470120-7	2014	C3 gene expression in bone was increased in the high bone turnover states of ovariectomy (OVX) or a receptor activator of NF-kappaB ligand (RANKL) injection, and blocking the action of C3a with the daily administration of SB290157 resulted in the attenuation of bone formation elevated by OVX and the exacerbation of bone loss.	SB 290157	222-230	TNF superfamily member 11	Homo sapiens	100-138
24470120-7	2014	C3 gene expression in bone was increased in the high bone turnover states of ovariectomy (OVX) or a receptor activator of NF-kappaB ligand (RANKL) injection, and blocking the action of C3a with the daily administration of SB290157 resulted in the attenuation of bone formation elevated by OVX and the exacerbation of bone loss.	SB 290157	222-230	complement C3	Homo sapiens	185-188
22089112-5	2012	We examined effects of C3a receptor inhibitor, SB290157, on Ang II-production in conditioned medium of VSMCs from SHR and WKY rats by a radioimmunoassay.	SB 290157	47-55	angiotensinogen	Rattus norvegicus	60-66
23713944-9	2014	Expression of osteopontin mRNA in MCs from SHR-SP and SHR was decreased with SB290157 treatment, whereas MC basal expression of alpha-SMA mRNA was decreased.	SB 290157	77-85	secreted phosphoprotein 1	Rattus norvegicus	14-25
23713944-10	2014	SB290157 significantly decreased the production of Ang II in MCs from SHR-SP and SHR.	SB 290157	0-8	angiotensinogen	Rattus norvegicus	51-57
22089112-8	2012	Relative to WKY VSMCs, SB290157 significantly increased the low expression of SM22alpha mRNA and decreased the high expression of osteopontin mRNA in SHR VSMCs.	SB 290157	23-31	transgelin	Rattus norvegicus	78-87
22089112-8	2012	Relative to WKY VSMCs, SB290157 significantly increased the low expression of SM22alpha mRNA and decreased the high expression of osteopontin mRNA in SHR VSMCs.	SB 290157	23-31	secreted phosphoprotein 1	Rattus norvegicus	130-141