diff --git a/src/data/drug-data.tsx b/src/data/drug-data.tsx
index bc9a7a132e133f66dcea7a3067bc23080fcfbc7c..6f4bdc6f8f249433e09fd2eb4d9385e407290bf5 100644
--- a/src/data/drug-data.tsx
+++ b/src/data/drug-data.tsx
@@ -16,11 +16,11 @@ export const drugdata: (Array<DrugDatensatz>)  = [
     {
         name: "About",
         picture: "...",
-        introduction: "CFTR modulators represent a significant advancement in CF treatment since they are small molecules improving the function of the defective CFTR protein in a mutation-specific way, which helps restore chloride ion transport across cell membranes. Notable pharmaceutical agents include Trikafta®, Symdeko®, Orkambi® and Kalydeco® [1]. These medications have been demonstrated to significantly improve lung function and reduce pulmonary exacerbations. However, they are expensive and may cause side effects such as liver enzyme elevations and cataracts in pediatric patients [2]. Furthermore, they are not suitable for all CF patients since only mutations which produce a CFTR channel can be supported by CFTR modulators, not those mutations which lead to a missing CFTR channel (knock out) [1], e.g. stop-mutations including p.Arg553Ter or p.Gly542Ter [3]. ",
+        introduction: "",
         examples: [
             {
-                title: "",
-                text: ""
+                title: "Introduction",
+                text: "CFTR modulators represent a significant advancement in CF treatment since they are small molecules improving the function of the defective CFTR protein in a mutation-specific way, which helps restore chloride ion transport across cell membranes. Notable pharmaceutical agents include Trikafta®, Symdeko®, Orkambi® and Kalydeco® [1]. These medications have been demonstrated to significantly improve lung function and reduce pulmonary exacerbations. However, they are expensive and may cause side effects such as liver enzyme elevations and cataracts in pediatric patients [2]. Furthermore, they are not suitable for all CF patients since only mutations which produce a CFTR channel can be supported by CFTR modulators, not those mutations which lead to a missing CFTR channel (knock out) [1], e.g. stop-mutations including p.Arg553Ter or p.Gly542Ter [3]. "
             },
             {
                 title: "",
@@ -35,11 +35,11 @@ export const drugdata: (Array<DrugDatensatz>)  = [
         examples: [
             {
                 title: "",
-                text: "string"
+                text: "Hallo hier soltle text stehen"
             },
             {
                 title: "",
-                text: "string"
+                text: "Moin"
             },
         ]
     },