PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
10432069-0	1999	Plasmodium falciparum: selection of serine 108 of dihydrofolate reductase during treatment of uncomplicated malaria with co-trimoxazole in Ugandan children.	Trimethoprim, Sulfamethoxazole Drug Combination	121-135	dihydrofolate reductase	Homo sapiens	50-73	
12018659-7	2002	The two patients whose isolates showed non-synonymous DHFR mutations were not exposed to DHFR inhibitors before they developed PCP and were treated successfully with co-trimoxazole.	Trimethoprim, Sulfamethoxazole Drug Combination	166-180	dihydrofolate reductase	Homo sapiens	54-58	
16014854-0	2005	Response of Plasmodium falciparum to cotrimoxazole therapy: relationship with plasma drug concentrations and dihydrofolate reductase and dihydropteroate synthase genotypes.	Trimethoprim, Sulfamethoxazole Drug Combination	37-50	dihydrofolate reductase	Homo sapiens	109-132	
16014854-1	2005	We assessed the efficacy of trimethoprim/sulfamethoxazole (TRM/SMX) in vivo in relation to the frequency of dihydrofolate reductase (dhfr) and dihydropteroate synthase (dhps) alleles in 45 Sudanese malaria patients.	Trimethoprim, Sulfamethoxazole Drug Combination	28-57	dihydrofolate reductase	Homo sapiens	108-131	
16014854-1	2005	We assessed the efficacy of trimethoprim/sulfamethoxazole (TRM/SMX) in vivo in relation to the frequency of dihydrofolate reductase (dhfr) and dihydropteroate synthase (dhps) alleles in 45 Sudanese malaria patients.	Trimethoprim, Sulfamethoxazole Drug Combination	28-57	dihydrofolate reductase	Homo sapiens	133-137	
16014854-1	2005	We assessed the efficacy of trimethoprim/sulfamethoxazole (TRM/SMX) in vivo in relation to the frequency of dihydrofolate reductase (dhfr) and dihydropteroate synthase (dhps) alleles in 45 Sudanese malaria patients.	Trimethoprim, Sulfamethoxazole Drug Combination	59-66	dihydrofolate reductase	Homo sapiens	108-131	
16014854-1	2005	We assessed the efficacy of trimethoprim/sulfamethoxazole (TRM/SMX) in vivo in relation to the frequency of dihydrofolate reductase (dhfr) and dihydropteroate synthase (dhps) alleles in 45 Sudanese malaria patients.	Trimethoprim, Sulfamethoxazole Drug Combination	59-66	dihydrofolate reductase	Homo sapiens	133-137	
16014854-8	2005	However, the presence of the triple mutant dhfr (Ile-51/Arg-59/Asn-108) with the dhps Gly-437 genotype in all recurring infections, suggests the importance of codon 59 and 437 alleles in susceptibility to TRM/SMX.	Trimethoprim, Sulfamethoxazole Drug Combination	205-212	dihydrofolate reductase	Homo sapiens	43-47	
10432069-2	1999	Selection towards a specific genotype at some codons of the DHFR and DHPS genes was observed in samples collected after exposure to co-trimoxazole drug pressure.	Trimethoprim, Sulfamethoxazole Drug Combination	132-146	dihydrofolate reductase	Homo sapiens	60-64	
33002448-10	2020	The high prevalence of quadruple dhps/dhfr mutants indicates strong antifolate drug pressure from SP or other drugs (e.g., co-trimoxazole).	Trimethoprim, Sulfamethoxazole Drug Combination	123-137	dihydrofolate reductase	Homo sapiens	38-42	
27647575-12	2016	Most likely, the sustained high prevalence of resistant parasites is due to the use of DHFR/DHPS inhibitors like trimethoprim-sulfamethoxazole (TS) for the treatment of and prophylaxis against bacterial infections among HIV infected individuals as well as the continued use of IPTp-SP within the East and Central African regions for malaria prevention among pregnant women.	Trimethoprim, Sulfamethoxazole Drug Combination	113-142	dihydrofolate reductase	Homo sapiens	87-91	
27647575-12	2016	Most likely, the sustained high prevalence of resistant parasites is due to the use of DHFR/DHPS inhibitors like trimethoprim-sulfamethoxazole (TS) for the treatment of and prophylaxis against bacterial infections among HIV infected individuals as well as the continued use of IPTp-SP within the East and Central African regions for malaria prevention among pregnant women.	Trimethoprim, Sulfamethoxazole Drug Combination	144-146	dihydrofolate reductase	Homo sapiens	87-91